Central regulation of body fluid homeostasis
Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na+ concentration ([Na+]) in body fluids is maintained at 135–145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na+ is vital for life becau...
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Published in | Proceedings of the Japan Academy, Series B Vol. 98; no. 7; pp. 283 - 324 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Ueno Park
The Japan Academy
29.07.2022
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Subjects | |
Online Access | Get full text |
ISSN | 0386-2208 1349-2896 1349-2896 |
DOI | 10.2183/pjab.98.016 |
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Abstract | Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na+ concentration ([Na+]) in body fluids is maintained at 135–145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na+ is vital for life because severe hyper- or hypotonicity elicits irreversible organ damage and lethal neurological trauma. To achieve “body fluid homeostasis” or “Na homeostasis”, the brain continuously monitors [Na+] in body fluids and controls water/salt intake and water/salt excretion by the kidneys. These physiological functions are primarily regulated based on information on [Na+] and relevant circulating hormones, such as angiotensin II, aldosterone, and vasopressin. In this review, we discuss sensing mechanisms for [Na+] and hormones in the brain that control water/salt intake behaviors, together with the responsible sensors (receptors) and relevant neural pathways. We also describe mechanisms in the brain by which [Na+] increases in body fluids activate the sympathetic neural activity leading to hypertension. |
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AbstractList | Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na+ concentration ([Na+]) in body fluids is maintained at 135-145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na+ is vital for life because severe hyper- or hypotonicity elicits irreversible organ damage and lethal neurological trauma. To achieve body fluid homeostasis or Na homeostasis, the brain continuously monitors [Na+] in body fluids and controls water/salt intake and water/salt excretion by the kidneys. These physiological functions are primarily regulated based on information on [Na+] and relevant circulating hormones, such as angiotensin II, aldosterone, and vasopressin. In this review, we discuss sensing mechanisms for [Na+] and hormones in the brain that control water/salt intake behaviors, together with the responsible sensors (receptors) and relevant neural pathways. We also describe mechanisms in the brain by which [Na+] increases in body fluids activate the sympathetic neural activity leading to hypertension. Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na + concentration ([Na + ]) in body fluids is maintained at 135–145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na + is vital for life because severe hyper- or hypotonicity elicits irreversible organ damage and lethal neurological trauma. To achieve “body fluid homeostasis” or “Na homeostasis”, the brain continuously monitors [Na + ] in body fluids and controls water/salt intake and water/salt excretion by the kidneys. These physiological functions are primarily regulated based on information on [Na + ] and relevant circulating hormones, such as angiotensin II, aldosterone, and vasopressin. In this review, we discuss sensing mechanisms for [Na + ] and hormones in the brain that control water/salt intake behaviors, together with the responsible sensors (receptors) and relevant neural pathways. We also describe mechanisms in the brain by which [Na + ] increases in body fluids activate the sympathetic neural activity leading to hypertension. Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na+ concentration ([Na+]) in body fluids is maintained at 135-145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na+ is vital for life because severe hyper- or hypotonicity elicits irreversible organ damage and lethal neurological trauma. To achieve "body fluid homeostasis" or "Na homeostasis", the brain continuously monitors [Na+] in body fluids and controls water/salt intake and water/salt excretion by the kidneys. These physiological functions are primarily regulated based on information on [Na+] and relevant circulating hormones, such as angiotensin II, aldosterone, and vasopressin. In this review, we discuss sensing mechanisms for [Na+] and hormones in the brain that control water/salt intake behaviors, together with the responsible sensors (receptors) and relevant neural pathways. We also describe mechanisms in the brain by which [Na+] increases in body fluids activate the sympathetic neural activity leading to hypertension.Extracellular fluids, including blood, lymphatic fluid, and cerebrospinal fluid, are collectively called body fluids. The Na+ concentration ([Na+]) in body fluids is maintained at 135-145 mM and is broadly conserved among terrestrial animals. Homeostatic osmoregulation by Na+ is vital for life because severe hyper- or hypotonicity elicits irreversible organ damage and lethal neurological trauma. To achieve "body fluid homeostasis" or "Na homeostasis", the brain continuously monitors [Na+] in body fluids and controls water/salt intake and water/salt excretion by the kidneys. These physiological functions are primarily regulated based on information on [Na+] and relevant circulating hormones, such as angiotensin II, aldosterone, and vasopressin. In this review, we discuss sensing mechanisms for [Na+] and hormones in the brain that control water/salt intake behaviors, together with the responsible sensors (receptors) and relevant neural pathways. We also describe mechanisms in the brain by which [Na+] increases in body fluids activate the sympathetic neural activity leading to hypertension. |
ArticleNumber | PJA9807B-01 |
Author | NODA, Masaharu MATSUDA, Takashi |
Author_xml | – sequence: 1 fullname: NODA, Masaharu organization: Homeostatic Mechanism Research Unit, Institute of Innovative Research, Tokyo Institute of Technology – sequence: 1 fullname: MATSUDA, Takashi organization: Homeostatic Mechanism Research Unit, Institute of Innovative Research, Tokyo Institute of Technology |
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Cites_doi | 10.1016/j.celrep.2021.108866 10.1016/0361-9230(93)90054-F 10.1152/ajpregu.1995.269.5.R1044 10.1164/rccm.201407-1262OC 10.1037/0735-7044.97.5.746 10.1037/0735-7044.104.2.365 10.1152/ajpregu.1987.252.1.R1 10.1016/0304-3940(93)90609-O 10.1016/0031-9384(84)90072-6 10.1016/0091-3057(75)90020-9 10.1016/j.neuron.2018.11.017 10.1152/ajpregu.1980.239.5.R382 10.1093/chemse/bjh105 10.1096/fj.10-165399 10.1016/j.neuron.2007.03.014 10.1152/ajpendo.00407.2011 10.1159/000071312 10.1002/cphy.c110020 10.1016/j.peptides.2010.02.020 10.3389/fnins.2015.00390 10.1053/ajkd.2002.34908 10.1152/japplphysiol.00825.2006 10.1016/j.neuron.2019.04.039 10.1038/nn.4463 10.1038/nrn.2017.71 10.1152/ajprenal.00200.2003 10.1038/250733a0 10.1096/fj.13-246868 10.1152/ajpregu.00311.2001 10.1016/S0092-8674(00)00143-4 10.1016/0006-8993(87)90128-4 10.1038/srep30168 10.1016/0006-8993(92)90749-Y 10.1007/978-3-642-55532-9_1 10.1016/j.tins.2013.08.004 10.1038/nrn1902 10.1152/ajpregu.00352.2015 10.1126/science.aav3932 10.1006/frne.1997.0153 10.1038/emboj.2008.233 10.1385/MB:24:1:27 10.1016/j.cell.2019.11.040 10.1152/ajpregu.00102.2014 10.1038/s41593-021-00850-4 10.1038/nn1614 10.1016/B978-0-08-027337-2.50045-6 10.1016/j.neuroscience.2006.04.015 10.1113/EP085349 10.1038/ncb1137 10.1016/j.brainres.2010.03.055 10.1073/pnas.0606894103 10.1385/MN:26:1:097 10.1111/j.0953-8194.2004.01184.x 10.1152/ajpregu.00063.2005 10.1016/0006-8993(81)90707-1 10.1002/cne.902930404 10.1186/1824-7288-36-78 10.1038/nature19756 10.1113/JP274667 10.1016/j.amjhyper.2004.10.032 10.1523/JNEUROSCI.3218-05.2006 10.1016/0167-0115(96)00058-4 10.1016/0006-8993(84)90140-9 10.1016/0028-3908(87)90118-3 10.1016/j.brainres.2010.11.075 10.1016/j.cmet.2010.09.011 10.1152/ajpregu.1999.276.4.R1180 10.1016/0361-9230(92)90234-O 10.1159/000125265 10.1016/S0006-8993(98)00530-7 10.1111/apha.13006 10.1016/0006-8993(94)91645-4 10.1056/NEJM200005183422006 10.1038/301628a0 10.1007/s00213-001-0932-y 10.1006/exnr.2002.8054 10.1016/j.neuroscience.2012.07.068 10.1006/exnr.2001.7776 10.1016/S0006-8993(99)01672-8 10.1152/ajpregu.1977.233.1.R44 10.1046/j.1365-2826.2003.00969.x 10.1073/pnas.1834556100 10.1523/JNEUROSCI.2208-19.2020 10.1016/0091-3057(76)90248-3 10.3389/fphys.2014.00436 10.1111/j.1365-2826.1992.tb00194.x 10.1152/ajpregu.1986.251.4.R762 10.1016/0006-8993(88)91633-2 10.1016/0006-8993(78)91125-3 10.1016/j.neuroscience.2008.06.011 10.1002/glia.22488 10.1113/jphysiol.1902.sp000920 10.1073/pnas.1616664113 10.1016/j.neuron.2016.11.021 10.1038/s41586-019-1053-2 10.1016/0079-6107(93)90009-9 10.1152/ajpcell.1997.272.1.C90 10.1210/jcem.86.12.8111 10.1016/0361-9230(85)90044-9 10.1002/cne.20993 10.1016/0091-3057(93)90382-4 10.1152/ajpcell.1996.271.5.C1629 10.1037/0735-7044.101.4.560 10.1038/sj.emboj.7600177 10.1038/nature18950 10.1016/j.neuroscience.2013.09.008 10.1016/0167-0115(88)90422-3 10.1016/j.neuroscience.2006.05.059 10.1016/0167-0115(96)00052-3 10.1111/bph.13659 10.1038/nature12041 10.1016/j.neuron.2017.11.041 10.1016/0361-9230(95)02084-5 10.1152/physrev.2001.81.2.629 10.1523/JNEUROSCI.0877-06.2006 10.1038/nrn2400 10.1152/ajpregu.00003.2008 10.1111/j.1523-1755.2004.66018.x 10.1038/s41586-020-2167-2 10.1097/HJH.0b013e32834f6de1 10.1038/s41593-017-0014-z 10.1152/ajpregu.00078.2015 10.1152/ajpregu.00242.2013 10.1002/cphy.c120001 10.1016/S0031-9384(03)00095-7 10.1016/0014-2999(88)90769-8 10.1016/S0006-8993(96)00615-4 10.1037/h0092457 10.1097/00001756-199309000-00003 10.1152/ajpheart.1984.247.3.H422 10.1073/pnas.81.5.1575 10.1152/ajprenal.2000.278.4.F585 10.1523/JNEUROSCI.2795-04.2004 10.1016/j.cmet.2013.02.018 10.1152/ajpregu.00486.2014 10.1016/S0092-8674(02)00670-0 10.1016/S0140-6736(01)36734-X 10.1016/j.celrep.2018.04.090 10.1038/nature01807 10.1016/j.neuroscience.2012.12.026 10.1037/h0024357 10.1126/science.6691151 10.1038/nature02196 10.1016/j.brainres.2006.07.091 10.1152/ajpregu.00869.2007 10.1016/j.cub.2016.11.019 10.1016/0306-4522(85)90281-7 10.1016/j.conb.2019.01.014 10.1161/HYPERTENSIONAHA.109.141994 10.3181/00379727-23-3107 10.1113/expphysiol.2006.035659 10.1152/physrev.00021.2001 10.1016/j.neuroscience.2005.02.004 10.1016/S0079-6123(08)64377-0 10.1016/j.neuroscience.2011.07.008 10.1523/JNEUROSCI.0237-05.2005 10.1016/j.cell.2020.07.031 10.1016/j.neulet.2003.12.040 10.1016/0006-8993(90)90245-7 10.1073/pnas.91.25.12022 10.1038/nature14108 10.1152/physrev.00036.2005 10.1038/35038090 10.1016/0006-8993(96)00277-6 10.1074/jbc.M003643200 10.1007/s13730-021-00638-2 10.1016/0006-8993(78)90619-4 10.1037/h0077759 10.1126/science.aan6747 10.1016/j.neuron.2017.09.014 10.1073/pnas.2009233117 10.1113/expphysiol.2007.039891 10.1002/(SICI)1096-9861(19990315)405:3<406::AID-CNE10>3.0.CO;2-F 10.1038/nature11905 10.1152/physrev.1998.78.3.583 10.1002/cne.902720408 10.1515/jbcpp-2014-0117 10.1016/0006-8993(94)01453-O 10.1016/j.brainres.2010.08.085 10.1016/j.jchemneu.2011.05.003 10.1038/nature25488 10.1111/bpa.12409 10.1152/ajpregu.00130.2003 10.1155/2013/175428 10.1159/000102536 10.1210/jendso/bvab048.1052 10.1016/j.pbb.2010.05.026 10.1093/chemse/bjn081 10.1152/ajpregu.1991.260.6.R1082 10.1038/35036318 10.1371/journal.pone.0022246 10.1152/jn.00177.2003 10.1152/ajpcell.00559.2002 10.1016/S0896-6273(00)00116-1 10.1056/NEJM200005253422107 10.1073/pnas.89.15.6828 10.1016/0031-9384(82)90348-1 10.1016/S0304-3940(02)00708-5 10.1074/jbc.M114.585067 10.1002/jcb.26552 10.1152/ajpregu.1987.253.1.R108 10.1210/endo-118-4-1726 10.1016/j.neuroscience.2011.02.019 10.1073/pnas.93.14.7397 10.1371/journal.pone.0126109 10.1210/en.2011-0006 10.1152/ajpcell.00601.2001 10.1152/ajpcell.00163.2011 10.1038/s41586-020-2821-8 10.1152/ajpregu.00391.2006 10.1096/fasebj.7.8.8500693 10.1016/S0306-4522(03)00316-6 10.1111/joa.12771 10.1152/ajpregu.1995.268.6.R1401 10.1038/477410a 10.1016/j.neuron.2014.12.048 10.1038/nature08783 10.1073/pnas.88.7.2956 10.1007/s11906-013-0385-9 10.1126/science.181.4105.1172 10.1073/pnas.0903695106 10.1056/NEJMoa1311989 10.1016/0361-9230(91)90148-D 10.1161/HYPERTENSIONAHA.115.05936 10.1046/j.1467-3010.2001.00097.x 10.1038/ki.1994.446 10.1016/S0031-9384(02)00751-5 10.1126/scisignal.2000769 10.1016/0165-0173(84)90012-2 10.1016/S0306-4522(00)00313-4 10.1038/nature14416 10.1073/pnas.2002825117 10.1016/S0304-3940(02)00203-3 10.1152/ajprenal.00191.2015 10.1002/cne.21025 10.1136/bmj.297.6644.319 10.1037/0735-7044.104.4.637 10.1152/ajpheart.01237.2003 10.1016/j.neuron.2010.04.017 10.1038/280490a0 10.1038/bjp.2008.92 10.1016/j.brainres.2010.11.028 10.3389/fnana.2017.00133 10.1002/cne.22442 10.1016/j.neuroscience.2009.08.048 10.1016/S0031-9384(75)80032-1 10.1159/000338163 10.1006/mcne.1993.1018 10.1016/j.celrep.2015.08.061 10.1016/S0169-328X(98)00308-8 10.1152/ajpregu.90560.2008 10.1152/ajpheart.00515.2002 10.1113/expphysiol.2008.044446 10.1016/j.physbeh.2008.08.004 10.1038/s41467-020-19191-0 10.1016/j.neures.2019.05.006 10.1113/jphysiol.1969.sp008848 10.3138/9781487578466-018 10.1016/0304-3940(85)90319-2 10.1016/j.bbr.2015.03.047 10.1210/en.130.4.1885 10.1016/S0006-8993(03)03015-4 10.1146/annurev.ph.39.030177.001153 10.1113/jphysiol.1970.sp009220 10.1016/j.neuroscience.2004.07.042 10.1016/j.neuron.2011.05.028 10.1152/ajpregu.00222.2013 10.1007/s11064-017-2336-3 10.1016/S0021-9258(18)43937-3 10.1016/0167-0115(84)90011-9 10.1523/ENEURO.0064-18.2018 10.1007/s00424-014-1662-4 10.1016/0361-9230(88)90223-7 10.1523/JNEUROSCI.3115-05.2006 10.1016/0196-9781(82)90113-9 10.1152/ajplegacy.1936.115.1.155 10.1016/j.cmet.2016.04.006 10.1073/pnas.1735416100 10.1016/j.bbr.2017.08.044 10.1146/annurev.biochem.68.1.425 10.1152/ajpregu.1998.275.5.R1431 10.1038/37610 10.1038/s41586-019-1066-x 10.1038/45230 10.1152/ajpregu.1980.238.5.R372 10.1210/endo-107-3-691 10.1007/s00424-020-02389-y 10.1038/nature12596 10.1016/0006-8993(89)91006-8 10.1073/pnas.82.24.8720 10.1152/ajpregu.00618.2005 10.1152/nips.01470.2003 10.1056/NEJMra064486 10.1126/science.1241812 10.1152/ajpregu.00251.2012 10.1152/ajpregu.1996.270.1.R162 10.1161/CIRCULATIONAHA.115.019341 10.1038/nn.4451 10.1590/S0001-37652004000100008 10.1016/0169-328X(94)00272-G 10.1007/s00213-016-4403-x 10.1152/ajpregu.00312.2015 10.1523/JNEUROSCI.20-20-07743.2000 10.1074/jbc.273.30.18677 10.1038/nn.4575 10.1037/0735-7044.104.4.643 10.1016/j.brainres.2009.08.094 10.1038/s41593-019-0573-2 10.1152/ajpregu.00460.2013 10.1038/nn0602-856 |
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References | 203) de Kloet, A.D., Liu, M., Rodríguez, V., Krause, E.G. and Sumners, C. (2015) Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control. Am. J. Physiol. Regul. Integr. Comp. Physiol. 309, R444–R458. 66) Tang, W., Strachan, R.T., Lefkowitz, R.J. and Rockman, H.A. (2014) Allosteric modulation of β-arrestin-biased angiotensin II type 1 receptor signaling by membrane stretch. J. Biol. Chem. 289, 28271–28283. 90) Hosutt, J.A., Rowland, N. and Stricker, E.M. (1981) Impaired drinking responses of rats with lesions on the subfornical organ. J. Comp. Physiol. Psychol. 95, 104–113. 73) Leib, D.E., Zimmerman, C.A. and Knight, Z.A. (2016) Thirst. Curr. Biol. 26, R1260–R1265. 211) Geerling, J.C. and Loewy, A.D. (2007) Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst. Am. J. Physiol. Regul. Integr. Comp. Physiol. 292, R1338–R1348. 279) Gimpl, G. and Fahrenholz, F. (2001) The oxytocin receptor system: structure, function, and regulation. Physiol. Rev. 81, 629–683. 91) Johnson, R.F., Beltz, T.G., Thunhorst, R.L. and Johnson, A.K. (2003) Investigations on the physiological controls of water and saline intake in C57BL/6 mice. Am. J. Physiol. Regul. Integr. Comp. Physiol. 285, R394–R403. 119) Allen, W.E., Chen, M.Z., Pichamoorthy, N., Tien, R.H., Pachitariu, M., Luo, L. et al. (2019) Thirst regulates motivated behavior through modulation of brainwide neural population dynamics. Science 364, 253. 50) Hollis, J.H., McKinley, M.J., D’Souza, M., Kampe, J. and Oldfield, B.J. (2008) The trajectory of sensory pathways from the lamina terminalis to the insular and cingulate cortex: a neuroanatomical framework for the generation of thirst. Am. J. Physiol. Regul. Integr. Comp. Physiol. 294, R1390–R1401. 142) Augustine, V., Lee, S. and Oka, Y. (2020) Neural control and modulation of thirst, sodium appetite, and hunger. Cell 180, 25–32. 291) Group, I.C.R. (1988) Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ 297, 319. 108) Fitzsimons, J.T. and Simons, B.J. (1969) The effect on drinking in the rat of intravenous infusion of angiotensin, given alone or in combination with other stimuli of thirst. J. Physiol. 203, 45–57. 245) Zardetto-Smith, A.M., Beltz, T.G. and Johnson, A.K. (1994) Role of the central nucleus of the amygdala and bed nucleus of the stria terminalis in experimentally-induced salt appetite. Brain Res. 645, 123–134. 31) Bookstein, C., Musch, M.W., DePaoli, A., Xie, Y., Rabenau, K., Villereal, M. et al. (1996) Characterization of the rat Na+/H+ exchanger isoform NHE4 and localization in rat hippocampus. Am. J. Physiol. 271, C1629–C1638. 165) Kojima, M., Hosoda, H., Date, Y., Nakazato, M., Matsuo, H. and Kangawa, K. (1999) Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402, 656–660. 283) Katoh, A., Fujihara, H., Ohbuchi, T., Onaka, T., Hashimoto, T., Kawata, M. et al. (2011) Highly visible expression of an oxytocin-monomeric red fluorescent protein 1 fusion gene in the hypothalamus and posterior pituitary of transgenic rats. Endocrinology 152, 2768–2774. 1) Cox, P.S., Denton, D.A., Mouw, D.R. and Tarjan, E. (1987) Natriuresis induced by localized perfusion within the third cerebral ventricle of sheep. Am. J. Physiol. 252, R1–R6. 43) Clapham, D.E. (2003) TRP channels as cellular sensors. Nature 426, 517–524. 46) Nishihara, E., Hiyama, T.Y. and Noda, M. (2011) Osmosensitivity of transient receptor potential vanilloid 1 is synergistically enhanced by distinct activating stimuli such as temperature and protons. PLoS One 6, e22246. 175) Nakamura, M., Katsuura, G., Nakao, K. and Imura, H. (1985) Antidipsogenic action of α-human atrial natriuretic polypeptide administered intracerebroventricularly in rats. Neurosci. Lett. 58, 1–6. 206) Sunn, N., McKinley, M.J. and Oldfield, B.J. (2003) Circulating angiotensin II activates neurones in circumventricular organs of the lamina terminalis that project to the bed nucleus of the stria terminalis. J. Neuroendocrinol. 15, 725–731. 243) Nogueiras, R., Romero-Picó, A., Vazquez, M.J., Novelle, M.G., López, M. and Diéguez, C. (2012) The opioid system and food intake: homeostatic and hedonic mechanisms. Obes. Facts 5, 196–207. 250) Chieng, B.C.H., Christie, M.J. and Osborne, P.B. (2006) Characterization of neurons in the rat central nucleus of the amygdala: Cellular physiology, morphology, and opioid sensitivity. J. Comp. Neurol. 497, 910–927. 195) Titze, J., Lang, R., Ilies, C., Schwind, K.H., Kirsch, K.A., Dietsch, P. et al. (2003) Osmotically inactive skin Na+ storage in rats. Am. J. Physiol. Renal Physiol. 285, F1108–F1117. 164) Xue, B., Johnson, A.K. and Hay, M. (2013) Sex differences in angiotensin II- and aldosterone-induced hypertension: the central protective effects of estrogen. Am. J. Physiol. Regul. Integr. Comp. Physiol. 305, R459–R463. 307) Bohlen, C.J., Chesler, A.T., Sharif-Naeini, R., Medzihradszky, K.F., Zhou, S., King, D. et al. (2011) A heteromeric Texas coral snake toxin targets acid-sensing ion channels to produce pain. Nature 479, 410–414. 210) Geerling, J.C. and Loewy, A.D. (2006) Aldosterone-sensitive NTS neurons are inhibited by saline ingestion during chronic mineralocorticoid treatment. Brain Res. 1115, 54–64. 47) Liedtke, W., Choe, Y., Martí-Renom, M.A., Bell, A.M., Denis, C.S., Sali, A. et al. (2000) Vanilloid receptor-related osmotically activated channel (VR-OAC), a candidate vertebrate osmoreceptor. Cell 103, 525–535. 130) de Avila, C., Chometton, S., Lenglos, C., Calvez, J., Gundlach, A.L. and Timofeeva, E. (2018) Differential effects of relaxin-3 and a selective relaxin-3 receptor agonist on food and water intake and hypothalamic neuronal activity in rats. Behav. Brain Res. 336, 135–144. 45) Bourque, C.W. (2008) Central mechanisms of osmosensation and systemic osmoregulation. Nat. Rev. Neurosci. 9, 519–531. 197) Wiig, H., Luft, F.C. and Titze, J.M. (2018) The interstitium conducts extrarenal storage of sodium and represents a third compartment essential for extracellular volume and blood pressure homeostasis. Acta Physiol. (Oxf.) 222, e13006. 135) Olszewski, P.K., Klockars, A., Schioth, H.B. and Levine, A.S. (2010) Oxytocin as feeding inhibitor: maintaining homeostasis in consummatory behavior. Pharmacol. Biochem. Behav. 97, 47–54. 262) Krukoff, T.L., Harris, K.H. and Jhamandas, J.H. (1993) Efferent projections from the parabrachial nucleus demonstrated with the anterograde tracer Phaseolus vulgaris leucoagglutinin. Brain Res. Bull. 30, 163–172. 54) Ahern, G.P., Brooks, I.M., Miyares, R.L. and Wang, X.B. (2005) Extracellular cations sensitize and gate capsaicin receptor TRPV1 modulating pain signaling. J. Neurosci. 25, 5109–5116. 177) Weisinger, R.S., Blair-West, J.R., Denton, D.A. and Tarjan, E. (1992) Central administration of atrial natriuretic peptide suppresses sodium and water intake of sheep. Brain Res. 579, 113–118. 139) Honda, T., Wada, E., Battey, J.F. and Wank, S.A. (1993) Differential gene expression of CCK(A) and CCK(B) receptors in the rat brain. Mol. Cell. Neurosci. 4, 143–154. 155) Allen, W.E., DeNardo, L.A., Chen, M.Z., Liu, C.D., Loh, K.M., Fenno, L.E. et al. (2017) Thirst-associated preoptic neurons encode an aversive motivational drive. Science 357, 1149–1155. 193) Heer, M., Baisch, F., Kropp, J., Gerzer, R. and Drummer, C. (2000) High dietary sodium chloride consumption may not induce body fluid retention in humans. Am. J. Physiol. Renal Physiol. 278, F585–F595. 32) Arena, E.A., Longo, W.E., Roberts, K.E., Geibel, P., Nateqi, J., Brandstetter, M. et al. (2012) Functional role of NHE4 as a pH regulator in rat and human colonic crypts. Am. J. Physiol. Cell Physiol. 302, C412–C418. 107) Johnson, A.K. and Schwob, J.E. (1975) Cephalic angiotensin receptors mediating drinking to systemic angiotensin II. Pharmacol. Biochem. Behav. 3, 1077–1084. 25) Rauh, A., Windischhofer, W., Kovacevic, A., DeVaney, T., Huber, E., Semlitsch, M. et al. (2008) Endothelin (ET)-1 and ET-3 promote expression of c-fos and c-jun in human choriocarcinoma via ET(B) receptor-mediated G(i)- and G(q)-pathways and MAP kinase activation. Br. J. Pharmacol. 154, 13–24. 68) Lefkowitz, R.J. (1998) G protein-coupled receptors: III. New roles for receptor kinases and β-arrestins in receptor signaling and desensitization. J. Biol. Chem. 273, 18677–18680. 111) Fitts, D.A. and Masson, D.B. (1990) Preoptic angiotensin and salt appetite. Behav. Neurosci. 104, 643–650. 10) Andersson, B. (1971) Thirst—and brain control of water balance. Am. Sci. 59, 408–415. 304) Stocker, S.D., Lang, S.M., Simmonds, S.S., Wenner, M.M. and Farquhar, W.B. (2015) Cerebrospinal fluid hypernatremia elevates sympathetic nerve activity and blood pressure via the rostral ventrolateral medulla. Hypertension 66, 1184–1190. 284) Boadle-Biber, M.C. (1993) Regulation of serotonin synthesis. Prog. Biophys. Mol. Biol. 60, 1–15. 277) Heck, G.L., Mierson, S. and DeSimone, J.A. (1984) Salt taste transduction occurs through an amiloride-sensitive sodium transport pathway. Science 223, 403–405. 182) Antunes-Rodrigues, J., Ramalho, M.J., Reis, L.C., Menani, J.V., Turrin, M.Q., Gutkowska, J. et al. (1991) Lesions of the hypothalamus and pituitary inhibit volume-expansion-induced release of atrial natriuretic peptide. Proc. Natl. Acad. Sci. U.S.A. 88, 2956–2960. 184) Bosler, O. and Descarries, L. (1988) Monoamine innervation of the organum vasculosum laminae terminalis (OVLT): a high resolution radioautographic study in the rat. J. Comp. Neurol. 272, 545–561. 181) Antunes-Rodrigues, J., McCann, S.M. and Samson, W.K. (1986) Central administration of atrial natriuretic factor inhibits saline preference in the rat. Endocrinology 118, 1726–1728. 19) Matsumoto, M., Hiyama, T.Y., Kuboyama, K., Suzuki, R., Fujikawa, A. and Noda, M. (2015) Channel properties of Nax expressed in neurons. PLoS One 10, e0126109. 92) Lind, R.W., Thunhorst, R.L. 230 110 231 111 232 112 233 113 234 114 235 115 236 116 237 117 238 118 239 119 10 11 12 13 14 15 16 17 18 19 240 120 241 121 242 1 122 243 2 123 244 3 124 245 4 125 246 5 126 247 6 127 248 7 128 249 8 129 9 20 21 22 23 24 25 26 27 28 29 250 130 251 131 252 132 253 133 254 134 135 256 136 257 137 258 138 259 139 30 31 32 33 34 35 36 37 38 39 260 140 261 141 262 142 263 143 264 144 265 145 266 146 267 147 268 148 269 149 40 41 42 43 44 45 46 47 48 49 270 150 271 151 272 152 273 153 274 154 275 155 276 156 277 157 278 158 279 159 50 51 52 53 54 55 56 57 58 59 280 160 281 161 282 162 283 163 284 164 285 165 286 287 167 288 168 289 169 60 61 62 63 64 65 66 67 68 69 290 170 291 171 292 172 293 173 294 174 295 175 296 176 297 177 298 178 J. Antunes-Rodrigues (181) 1986 T. Yamamoto (255) 1993 299 179 70 71 72 73 74 75 76 77 78 79 180 182 183 184 185 186 187 188 189 80 81 82 83 84 85 86 87 88 89 190 191 192 193 194 195 196 197 198 199 90 91 92 93 94 95 96 97 98 99 M. Tschop (166) 2000 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 216 217 218 219 220 100 221 101 222 102 223 103 224 104 225 105 226 106 227 107 228 108 229 109 |
References_xml | – reference: 120) Bayliss, W.M. and Starling, E.H. (1902) The mechanism of pancreatic secretion. J. Physiol. 28, 325–353. – reference: 185) Stein, J.M., Lind, R.W. and Johnson, A.K. (1987) Central serotonergic influences on renal electrolyte and water excretion. Neuropharmacology 26, 1685–1692. – reference: 63) Mederos y Schnitzler, M., Storch, U., Meibers, S., Nurwakagari, P., Breit, A., Essin, K. et al. (2008) Gq-coupled receptors as mechanosensors mediating myogenic vasoconstriction. EMBO J. 27, 3092–3103. – reference: 247) Wang, Q., Li, J.R., Yang, X.J., Chen, K., Sun, B. and Yan, J.Q. (2012) Inhibitory effect of activation of GABAA receptor in the central nucleus of amygdala on the sodium intake in the sodium-depleted rat. Neuroscience 223, 277–284. – reference: 113) Weisinger, R.S., Denton, D.A., Di Nicolantonio, R., Hards, D.K., McKinley, M.J., Oldfield, B. et al. (1990) Subfornical organ lesion decreases sodium appetite in the sodium-depleted rat. Brain Res. 526, 23–30. – reference: 138) Matsuda, T., Hiyama, T.Y., Kobayashi, K., Kobayashi, K. and Noda, M. (2020) Distinct CCK-positive SFO neurons are involved in persistent or transient suppression of water intake. Nat. Commun. 11, 5692. – reference: 286) Lima, H.R., Cavalcante-Lima, H.R., Cedraz-Mercez, P.L., Costa, E.S.R.H., Olivares, E.L., Badaue-Passos, D. Jr. et al. (2004) Brain serotonin depletion enhances the sodium appetite induced by sodium depletion or beta-adrenergic stimulation. An. Acad. Bras. Cienc. 76, 85–92. – reference: 12) McKinley, M.J., Denton, D.A. and Weisinger, R.S. (1978) Sensors for antidiuresis and thirst—osmoreceptors or CSF sodium detectors? Brain Res. 141, 89–103. – reference: 302) Choe, K.Y., Han, S.Y., Gaub, P., Shell, B., Voisin, D.L., Knapp, B.A. et al. (2015) High salt intake increases blood pressure via BDNF-mediated downregulation of KCC2 and impaired baroreflex inhibition of vasopressin neurons. Neuron 85, 549–560. – reference: 168) Cabral, A., Fernandez, G. and Perello, M. (2013) Analysis of brain nuclei accessible to ghrelin present in the cerebrospinal fluid. Neuroscience 253, 406–415. – reference: 197) Wiig, H., Luft, F.C. and Titze, J.M. (2018) The interstitium conducts extrarenal storage of sodium and represents a third compartment essential for extracellular volume and blood pressure homeostasis. Acta Physiol. (Oxf.) 222, e13006. – reference: 5) Johnson, A.K. and Gross, P.M. (1993) Sensory circumventricular organs and brain homeostatic pathways. FASEB J. 7, 678–686. – reference: 223) Curtis, K.S., Verbalis, J.G. and Stricker, E.M. (1996) Area postrema lesions in rats appear to disrupt rapid feedback inhibition of fluid intake. Brain Res. 726, 31–38. – reference: 42) Montell, C., Birnbaumer, L. and Flockerzi, V. (2002) The TRP channels, a remarkably functional family. Cell 108, 595–598. – reference: 35) Miller, R.L., Wang, M.H., Gray, P.A., Salkoff, L.B. and Loewy, A.D. (2013) ENaC-expressing neurons in the sensory circumventricular organs become c-Fos activated following systemic sodium changes. Am. J. Physiol. Regul. Integr. Comp. Physiol. 305, R1141–R1152. – reference: 224) Geerling, J.C. and Loewy, A.D. (2006) Aldosterone-sensitive neurons in the nucleus of the solitary tract: efferent projections. J. Comp. Neurol. 497, 223–250. – reference: 268) Menani, J.V., Barbosa, S.P., De Luca, L.A., De Gobbi, J.I.F. and Johnson, A.K. (2002) Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite. Am. J. Physiol. Regul. Integr. Comp. Physiol. 282, R837–R841. – reference: 161) Krause, E.G., Curtis, K.S., Davis, L.M., Stowe, J.R. and Contreras, R.J. (2003) Estrogen influences stimulated water intake by ovariectomized female rats. Physiol. Behav. 79, 267–274. – reference: 26) Robin, P., Boulven, I., Desmyter, C., Harbon, S. and Leiber, D. (2002) ET-1 stimulates ERK signaling pathway through sequential activation of PKC and Src in rat myometrial cells. Am. J. Physiol. Cell Physiol. 283, C251–C260. – reference: 75) McKinley, M.J. and Johnson, A.K. (2004) The physiological regulation of thirst and fluid intake. News Physiol. Sci. 19, 1–6. – reference: 171) Antunes-Rodrigues, J., McCann, S.M., Rogers, L.C. and Samson, W.K. (1985) Atrial natriuretic factor inhibits dehydration- and angiotensin II-induced water intake in the conscious, unrestrained rat. Proc. Natl. Acad. Sci. U.S.A. 82, 8720. – reference: 254) Kobashi, M., Ichikawa, H., Sugimoto, T. and Adachi, A. (1993) Response of neurons in the solitary tract nucleus, area postrema and lateral parabrachial nucleus to gastric load of hypertonic saline. Neurosci. Lett. 158, 47–50. – reference: 172) Masotto, C. and Negro-Vilar, A. (1985) Inhibition of spontaneous or angiotensin II-stimulated water intake by atrial natriuretic factor. Brain Res. Bull. 15, 523–526. – reference: 76) Zimmerman, C.A., Leib, D.E. and Knight, Z.A. (2017) Neural circuits underlying thirst and fluid homeostasis. Nat. Rev. Neurosci. 18, 459–469. – reference: 252) Andrade-Franzé, G.M.F., Andrade, C.A.F., De Luca, L.A., De Paula, P.M., Colombari, D.S.A. and Menani, J.V. (2010) Lesions in the central amygdala impair sodium intake induced by the blockade of the lateral parabrachial nucleus. Brain Res. 1332, 57–64. – reference: 284) Boadle-Biber, M.C. (1993) Regulation of serotonin synthesis. Prog. Biophys. Mol. Biol. 60, 1–15. – reference: 233) Smith, C.M. and Lawrence, A.J. (2018) Salt Appetite, and the Influence of Opioids. Neurochem. Res. 43, 12–18. – reference: 248) Yan, J., Li, J., Yan, J., Sun, H., Wang, Q., Chen, K. et al. (2013) Activation of μ-opioid receptors in the central nucleus of the amygdala induces hypertonic sodium intake. Neuroscience 233, 28–43. – reference: 102) Paul, M., Poyan Mehr, A. and Kreutz, R. (2006) Physiology of local renin-angiotensin systems. Physiol. Rev. 86, 747–803. – reference: 139) Honda, T., Wada, E., Battey, J.F. and Wank, S.A. (1993) Differential gene expression of CCK(A) and CCK(B) receptors in the rat brain. Mol. Cell. Neurosci. 4, 143–154. – reference: 146) Davern, P.J. (2014) A role for the lateral parabrachial nucleus in cardiovascular function and fluid homeostasis. Front. Physiol. 5, 436. – reference: 131) Smith, C.M., Shen, P.J., Banerjee, A., Bonaventure, P., Ma, S., Bathgate, R.A. et al. (2010) Distribution of relaxin-3 and RXFP3 within arousal, stress, affective, and cognitive circuits of mouse brain. J. Comp. Neurol. 518, 4016–4045. – reference: 165) Kojima, M., Hosoda, H., Date, Y., Nakazato, M., Matsuo, H. and Kangawa, K. (1999) Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402, 656–660. – reference: 201) Epstein, A.N. (1982) Mineralocorticoids and cerebral angiotensin may act together to produce sodium appetite. Peptides 3, 493–494. – reference: 128) Sherwood, O.D., Crnekovic, V.E., Gordon, W.L. and Rutherford, J.E. (1980) Radioimmunoassay of relaxin throughout pregnancy and during parturition in the rat. Endocrinology 107, 691–698. – reference: 264) Jhamandas, J.H., Harris, K.H., Petrov, T. and Krukoff, T.L. (1992) Characterization of the Parabrachial Nucleus Input to the Hypothalamic Paraventricular Nucleus in the Rat. J. Neuroendocrinol. 4, 461–471. – reference: 294) de Wardener, H.E., He, F.J. and MacGregor, G.A. (2004) Plasma sodium and hypertension. Kidney Int. 66, 2454–2466. – reference: 93) Watanabe, H., Vriens, J., Prenen, J., Droogmans, G., Voets, T. and Nilius, B. (2003) Anandamide and arachidonic acid use epoxyeicosatrienoic acids to activate TRPV4 channels. Nature 424, 434–438. – reference: 115) Leib, D.E., Zimmerman, C.A., Poormoghaddam, A., Huey, E.L., Ahn, J.S., Lin, Y.C. et al. (2017) The forebrain thirst circuit drives drinking through negative reinforcement. Neuron 96, 1272–1281.e1274. – reference: 309) Hiyama, T.Y., Matsuda, S., Fujikawa, A., Matsumoto, M., Watanabe, E., Kajiwara, H. et al. (2010) Autoimmunity to the sodium-level sensor in the brain causes essential hypernatremia. Neuron 66, 508–522. – reference: 142) Augustine, V., Lee, S. and Oka, Y. (2020) Neural control and modulation of thirst, sodium appetite, and hunger. Cell 180, 25–32. – reference: 118) Abbott, S.B.G. and Saper, C.B. (2017) Median preoptic glutamatergic neurons promote thermoregulatory heat loss and water consumption in mice. J. Physiol. 595, 6569–6583. – reference: 182) Antunes-Rodrigues, J., Ramalho, M.J., Reis, L.C., Menani, J.V., Turrin, M.Q., Gutkowska, J. et al. (1991) Lesions of the hypothalamus and pituitary inhibit volume-expansion-induced release of atrial natriuretic peptide. Proc. Natl. Acad. Sci. U.S.A. 88, 2956–2960. – reference: 217) Daniels, D., Mietlicki, E.G., Nowak, E.L. and Fluharty, S.J. (2009) Angiotensin II stimulates water and NaCl intake through separate cell signalling pathways in rats. Exp. Physiol. 94, 130–137. – reference: 23) Hindmarch, C., Fry, M., Yao, S.T., Smith, P.M., Murphy, D. and Ferguson, A.V. (2008) Microarray analysis of the transcriptome of the subfornical organ in the rat: regulation by fluid and food deprivation. Am. J. Physiol. Regul. Integr. Comp. Physiol. 295, R1914–R1920. – reference: 273) Gasparini, S., de Luca, L.A., Colombari, D.S.A., de Paula, P.M., Barbosa, S.P. and Menani, J.V. (2009) Adrenergic mechanisms of the Kölliker-Fuse/A7 area on the control of water and sodium intake. Neuroscience 164, 370–379. – reference: 232) Lee, S., Augustine, V., Zhao, Y., Ebisu, H., Ho, B., Kong, D. et al. (2019) Chemosensory modulation of neural circuits for sodium appetite. Nature 568, 93–97. – reference: 225) Evans, L.C., Ivy, J.R., Wyrwoll, C., McNairn, J.A., Menzies, R.I., Christensen, T.H. et al. (2016) Conditional deletion of Hsd11b2 in the brain causes salt appetite and hypertension. Circulation 133, 1360–1370. – reference: 237) Zhang, M. and Kelley, A.E. (2002) Intake of saccharin, salt, and ethanol solutions is increased by infusion of a mu opioid agonist into the nucleus accumbens. Psychopharmacology (Berl) 159, 415–423. – reference: 269) De luca, L.A., Barbosa, S.P. and Menani, J.V. (2003) Brain serotonin blockade and paradoxical salt intake in rats. Neuroscience 121, 1055–1061. – reference: 119) Allen, W.E., Chen, M.Z., Pichamoorthy, N., Tien, R.H., Pachitariu, M., Luo, L. et al. (2019) Thirst regulates motivated behavior through modulation of brainwide neural population dynamics. Science 364, 253. – reference: 145) Zocchi, D., Wennemuth, G. and Oka, Y. (2017) The cellular mechanism for water detection in the mammalian taste system. Nat. Neurosci. 20, 927–933. – reference: 141) Augustine, V., Ebisu, H., Zhao, Y., Lee, S., Ho, B., Mizuno, G.O. et al. (2019) Temporally and spatially distinct thirst satiation signals. Neuron 103, 242–249.e244. – reference: 262) Krukoff, T.L., Harris, K.H. and Jhamandas, J.H. (1993) Efferent projections from the parabrachial nucleus demonstrated with the anterograde tracer Phaseolus vulgaris leucoagglutinin. Brain Res. Bull. 30, 163–172. – reference: 125) Lee, L.T., Ng, S.Y., Chu, J.Y., Sekar, R., Harikumar, K.G., Miller, L.J. et al. (2014) Transmembrane peptides as unique tools to demonstrate the in vivo action of a cross-class GPCR heterocomplex. FASEB J. 28, 2632–2644. – reference: 51) Liedtke, W. and Friedman, J.M. (2003) Abnormal osmotic regulation in trpv4−/− mice. Proc. Natl. Acad. Sci. U.S.A. 100, 13698–13703. – reference: 8) Peruzzo, M., Milani, G.P., Garzoni, L., Longoni, L., Simonetti, G.D., Bettinelli, A. et al. (2010) Body fluids and salt metabolism - part II. Ital. J. Pediatr. 36, 78. – reference: 164) Xue, B., Johnson, A.K. and Hay, M. (2013) Sex differences in angiotensin II- and aldosterone-induced hypertension: the central protective effects of estrogen. Am. J. Physiol. Regul. Integr. Comp. Physiol. 305, R459–R463. – reference: 206) Sunn, N., McKinley, M.J. and Oldfield, B.J. (2003) Circulating angiotensin II activates neurones in circumventricular organs of the lamina terminalis that project to the bed nucleus of the stria terminalis. J. Neuroendocrinol. 15, 725–731. – reference: 239) Pavan, C.G., Roncari, C.F., Barbosa, S.P., De Paula, P.M., Colombari, D.S., De Luca, L.A. Jr. et al. (2015) Activation of μ opioid receptors in the LPBN facilitates sodium intake in rats. Behav. Brain Res. 288, 20–25. – reference: 106) Grobe, J.L., Grobe, C.L., Beltz, T.G., Westphal, S.G., Morgan, D.A., Xu, D. et al. (2010) The brain Renin-angiotensin system controls divergent efferent mechanisms to regulate fluid and energy balance. Cell Metab. 12, 431–442. – reference: 288) Park, S., Williams, K.W., Liu, C. and Sohn, J.W. (2020) A neural basis for tonic suppression of sodium appetite. Nat. Neurosci. 23, 423–432. – reference: 147) Menani, J.V., De Luca, L.A. Jr. and Johnson, A.K. (2014) Role of the lateral parabrachial nucleus in the control of sodium appetite. Am. J. Physiol. Regul. Integr. Comp. Physiol. 306, R201–R210. – reference: 263) Jhamandas, J.H., Petrov, T., Harris, K.H., Vu, T. and Krukoff, T.L. (1996) Parabrachial nucleus projection to the amygdala in the rat: Electrophysiological and anatomical observations. Brain Res. Bull. 39, 115–126. – reference: 53) Zheng, J. (2013) Molecular mechanism of TRP channels. Compr. Physiol. 3, 221–242. – reference: 103) Abdelaal, A.E., Mercer, P.F. and Mogenson, G.J. (1976) Plasma angiotensin II levels and water intake following β-adrenergic stimulation, hypovolemia, cellular dehydration and water deprivation. Pharmacol. Biochem. Behav. 4, 317–321. – reference: 123) Ng, S.S., Yung, W.H. and Chow, B.K. (2002) Secretin as a neuropeptide. Mol. Neurobiol. 26, 97–107. – reference: 137) Willis, G.L., Hansky, J. and Smith, G.C. (1984) Ventricular, paraventricular and circumventricular structures involved in peptide-induced satiety. Regul. Pept. 9, 87–99. – reference: 158) Mandelblat-Cerf, Y., Kim, A., Burgess, C.R., Subramanian, S., Tannous, B.A., Lowell, B.B. et al. (2017) Bidirectional anticipation of future osmotic challenges by vasopressin neurons. Neuron 93, 57–65. – reference: 211) Geerling, J.C. and Loewy, A.D. (2007) Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst. Am. J. Physiol. Regul. Integr. Comp. Physiol. 292, R1338–R1348. – reference: 65) Rakesh, K., Yoo, B., Kim, I.-M., Salazar, N., Kim, K.-S. and Rockman, H.A. (2010) β-Arrestin-biased agonism of the angiotensin receptor induced by mechanical stress. Sci. Signal. 3, ra46. – reference: 90) Hosutt, J.A., Rowland, N. and Stricker, E.M. (1981) Impaired drinking responses of rats with lesions on the subfornical organ. J. Comp. Physiol. Psychol. 95, 104–113. – reference: 208) Terenzi, M.G. and Ingram, C.D. (1995) A combined immunocytochemical and retrograde tracing study of noradrenergic connections between the caudal medulla and bed nuclei of the stria terminalis. Brain Res. 672, 289–297. – reference: 144) Winzeler, B.F., Sailer, C.O., Coynel, D., Deborah, V., Davide, Z., Urwyler, S. et al. (2021) GLP1 receptor agonists reduce fluid intake in primary polydipsia. J. Endocr. Soc. 5, A514–A515. – reference: 287) Menani, J.V., Colombari, D.S., Beltz, T.G., Thunhorst, R.L. and Johnson, A.K. (1998) Salt appetite: interaction of forebrain angiotensinergic and hindbrain serotonergic mechanisms. Brain Res. 801, 29–35. – reference: 155) Allen, W.E., DeNardo, L.A., Chen, M.Z., Liu, C.D., Loh, K.M., Fenno, L.E. et al. (2017) Thirst-associated preoptic neurons encode an aversive motivational drive. Science 357, 1149–1155. – reference: 71) Adrogué, H.J. and Madias, N.E. (2000) Hypernatremia. N. Engl. J. Med. 342, 1493–1499. – reference: 20) Hiyama, T.Y., Watanabe, E., Okado, H. and Noda, M. (2004) The subfornical organ is the primary locus of sodium-level sensing by Nax sodium channels for the control of salt-intake behavior. J. Neurosci. 24, 9276. – reference: 97) Mann, J.F., Johnson, A.K. and Ganten, D. (1980) Plasma angiotensin II: dipsogenic levels and angiotensin-generating capacity of renin. Am. J. Physiol. 238, R372–R377. – reference: 212) Li, Z., Iwai, M., Wu, L., Shiuchi, T., Jinno, T., Cui, T.X. et al. (2003) Role of AT2 receptor in the brain in regulation of blood pressure and water intake. Am. J. Physiol. Heart Circ. Physiol. 284, H116–H121. – reference: 258) Ciriello, J., Lawrence, D. and Pittman, Q.J. (1984) Electrophysiological identification of neurons in the parabrachial nucleus projecting directly to the hypothalamus in the rat. Brain Res. 322, 388–392. – reference: 276) Tanaka, J., Hayashi, Y., Yamato, K., Miyakubo, H. and Nomura, M. (2004) Involvement of serotonergic systems in the lateral parabrachial nucleus in sodium and water intake: a microdialysis study in the rat. Neurosci. Lett. 357, 41–44. – reference: 116) Vong, L., Ye, C., Yang, Z., Choi, B., Chua, S. Jr. and Lowell, B.B. (2011) Leptin action on GABAergic neurons prevents obesity and reduces inhibitory tone to POMC neurons. Neuron 71, 142–154. – reference: 226) Jarvie, B.C. and Palmiter, R.D. (2017) HSD2 neurons in the hindbrain drive sodium appetite. Nat. Neurosci. 20, 167–169. – reference: 73) Leib, D.E., Zimmerman, C.A. and Knight, Z.A. (2016) Thirst. Curr. Biol. 26, R1260–R1265. – reference: 249) Zhu, W. and Pan, Z.Z. (2005) μ-opioid-mediated inhibition of glutamate synaptic transmission in rat central amygdala neurons. Neuroscience 133, 97–103. – reference: 47) Liedtke, W., Choe, Y., Martí-Renom, M.A., Bell, A.M., Denis, C.S., Sali, A. et al. (2000) Vanilloid receptor-related osmotically activated channel (VR-OAC), a candidate vertebrate osmoreceptor. Cell 103, 525–535. – reference: 257) Norgren, R. (1981) The central organization of the gustatory and visceral afferent systems in the nucleus of the solitary tract. Brain mechanisms of sensation, 143–160. – reference: 34) Chambrey, R., Achard, J.M. and Warnock, D.G. (1997) Heterologous expression of rat NHE4: a highly amiloride-resistant Na+/H+ exchanger isoform. Am. J. Physiol. 272, C90–C98. – reference: 304) Stocker, S.D., Lang, S.M., Simmonds, S.S., Wenner, M.M. and Farquhar, W.B. (2015) Cerebrospinal fluid hypernatremia elevates sympathetic nerve activity and blood pressure via the rostral ventrolateral medulla. Hypertension 66, 1184–1190. – reference: 70) Fitzsimons, J.T. (1998) Angiotensin, thirst, and sodium appetite. Physiol. Rev. 78, 583–686. – reference: 58) Taylor, A.C., McCarthy, J.J. and Stocker, S.D. (2008) Mice lacking the transient receptor vanilloid potential 1 channel display normal thirst responses and central Fos activation to hypernatremia. Am. J. Physiol. Regul. Integr. Comp. Physiol. 294, R1285–R1293. – reference: 221) Contreras, R.J. and Stetson, P.W. (1981) Changes in salt intake after lesions of the area postrema and the nucleus of the solitary tract in rats. Brain Res. 211, 355–366. – reference: 305) Escoubas, P., De Weille, J.R., Lecoq, A., Diochot, S., Waldmann, R., Champigny, G. et al. (2000) Isolation of a tarantula toxin specific for a class of proton-gated Na+ channels. J. Biol. Chem. 275, 25116–25121. – reference: 272) De Gobbi, J.I.F., Beltz, T.G., Johnson, R.F., Menani, J.V., Thunhorst, R.L. and Johnson, A.K. (2009) Non-NMDA receptors in the lateral parabrachial nucleus modulate sodium appetite. Brain Res. 1301, 44–51. – reference: 167) Wren, A.M., Seal, L.J., Cohen, M.A., Brynes, A.E., Frost, G.S., Murphy, K.G. et al. (2001) Ghrelin enhances appetite and increases food intake in humans. J. Clin. Endocrinol. Metab. 86, 5992–5995. – reference: 83) Simpson, J.B. and Routtenberg, A. (1973) Subfornical organ: site of drinking elicitation by angiotensin II. Science 181, 1172. – reference: 46) Nishihara, E., Hiyama, T.Y. and Noda, M. (2011) Osmosensitivity of transient receptor potential vanilloid 1 is synergistically enhanced by distinct activating stimuli such as temperature and protons. PLoS One 6, e22246. – reference: 313) Eiselt, A.K., Chen, S., Chen, J., Arnold, J., Kim, T., Pachitariu, M. et al. (2021) Hunger or thirst state uncertainty is resolved by outcome evaluation in medial prefrontal cortex to guide decision-making. Nat. Neurosci. 24, 907–912. – reference: 149) Ryan, P.J., Ross, S.I., Campos, C.A., Derkach, V.A. and Palmiter, R.D. (2017) Oxytocin-receptor-expressing neurons in the parabrachial nucleus regulate fluid intake. Nat. Neurosci. 20, 1722–1733. – reference: 246) Covian, M.R., Antunes-Rodrigues, J., Gentil, C.G., Saad, W.A., Camargo, L.A. and Neto, C.R.S. (2019) Central control of salt balance. In Neural Integration of Physiological Mechanisms and Behaviour (eds. Mogenson, G. and Calaresu, F.). University of Toronto Press, Toronto, pp. 267–282. – reference: 275) Menezes, M.F., Barbosa, S.P., De Andrade, C.A.F., Menani, J.V. and De Paula, P.M. (2011) Purinergic mechanisms of lateral parabrachial nucleus facilitate sodium depletion-induced NaCl intake. Brain Res. 1372, 49–58. – reference: 153) Hsu, T.M., Bazzino, P., Hurh, S.J., Konanur, V.R., Roitman, J.D. and Roitman, M.F. (2020) Thirst recruits phasic dopamine signaling through subfornical organ neurons. Proc. Natl. Acad. Sci. U.S.A. 117, 30744–30754. – reference: 265) Menani, J.V. and Johnson, A.K. (1995) Lateral parabrachial serotonergic mechanisms: Angiotensin-induced pressor and drinking responses. Am. J. Physiol. Regul. Integr. Comp. Physiol. 269, R1044–R1049. – reference: 195) Titze, J., Lang, R., Ilies, C., Schwind, K.H., Kirsch, K.A., Dietsch, P. et al. (2003) Osmotically inactive skin Na+ storage in rats. Am. J. Physiol. Renal Physiol. 285, F1108–F1117. – reference: 67) Wang, J., Hanada, K., Gareri, C. and Rockman, H.A. (2018) Mechanoactivation of the angiotensin II type 1 receptor induces β-arrestin-biased signaling through Gα(i) coupling. J. Cell. Biochem. 119, 3586–3597. – reference: 188) McCance, R. (1936) Experimental human salt deficiency. Lancet 1, 823–830. – reference: 36) Amin, M.S., Wang, H.W., Reza, E., Whitman, S.C., Tuana, B.S. and Leenen, F.H. (2005) Distribution of epithelial sodium channels and mineralocorticoid receptors in cardiovascular regulatory centers in rat brain. Am. J. Physiol. Regul. Integr. Comp. Physiol. 289, R1787–R1797. – reference: 64) Zou, Y., Akazawa, H., Qin, Y., Sano, M., Takano, H., Minamino, T. et al. (2004) Mechanical stress activates angiotensin II type 1 receptor without the involvement of angiotensin II. Nat. Cell Biol. 6, 499–506. – reference: 82) Noda, M. and Hiyama, T.Y. (2015) Sodium sensing in the brain. Pflugers Arch. 467, 465–474. – reference: 187) Reis, L.C., Ramalho, M.J., Favaretto, A.L., Gutkowska, J., McCann, S.M. and Antunes-Rodrigues, J. (1994) Participation of the ascending serotonergic system in the stimulation of atrial natriuretic peptide release. Proc. Natl. Acad. Sci. U.S.A. 91, 12022–12026. – reference: 190) Contreras, R.J. and Hatton, G.I. (1975) Gustatory adaptation as an explanation for dietary-induced sodium appetite. Physiol. Behav. 15, 569–576. – reference: 15) Watanabe, E., Fujikawa, A., Matsunaga, H., Yasoshima, Y., Sako, N., Yamamoto, T. et al. (2000) Nav2/NaG channel is involved in control of salt-intake behavior in the CNS. J. Neurosci. 20, 7743–7751. – reference: 25) Rauh, A., Windischhofer, W., Kovacevic, A., DeVaney, T., Huber, E., Semlitsch, M. et al. (2008) Endothelin (ET)-1 and ET-3 promote expression of c-fos and c-jun in human choriocarcinoma via ET(B) receptor-mediated G(i)- and G(q)-pathways and MAP kinase activation. Br. J. Pharmacol. 154, 13–24. – reference: 54) Ahern, G.P., Brooks, I.M., Miyares, R.L. and Wang, X.B. (2005) Extracellular cations sensitize and gate capsaicin receptor TRPV1 modulating pain signaling. J. Neurosci. 25, 5109–5116. – reference: 57) Kinsman, B., Cowles, J., Lay, J., Simmonds, S.S., Browning, K.N. and Stocker, S.D. (2014) Osmoregulatory thirst in mice lacking the transient receptor potential vanilloid type 1 (TRPV1) and/or type 4 (TRPV4) receptor. Am. J. Physiol. Regul. Integr. Comp. Physiol. 307, R1092–R1100. – reference: 216) Wei, H., Ahn, S., Shenoy, S.K., Karnik, S.S., Hunyady, L., Luttrell, L.M. et al. (2003) Independent β-arrestin 2 and G protein-mediated pathways for angiotensin II activation of extracellular signal-regulated kinases 1 and 2. Proc. Natl. Acad. Sci. U.S.A. 100, 10782–10787. – reference: 14) Goldin, A.L., Barchi, R.L., Caldwell, J.H., Hofmann, F., Howe, J.R., Hunter, J.C. et al. (2000) Nomenclature of voltage-gated sodium channels. Neuron 28, 365–368. – reference: 236) Lucas, L.R., Grillo, C.A. and McEwen, B.S. (2007) Salt appetite in sodium-depleted or sodium-replete conditions: possible role of opioid receptors. Neuroendocrinology 85, 139–147. – reference: 94) Roman, R.J. (2002) P-450 metabolites of arachidonic acid in the control of cardiovascular function. Physiol. Rev. 82, 131–185. – reference: 129) Otsubo, H., Onaka, T., Suzuki, H., Katoh, A., Ohbuchi, T., Todoroki, M. et al. (2010) Centrally administered relaxin-3 induces Fos expression in the osmosensitive areas in rat brain and facilitates water intake. Peptides 31, 1124–1130. – reference: 274) De Oliveira, L.B., Kimura, E.H., Callera, J.C., De Luca, L.A., Colombari, D.S.A. and Menani, J.V. (2011) Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride and sucrose intake in rats. Neuroscience 183, 160–170. – reference: 105) Premer, C., Lamondin, C., Mitzey, A., Speth, R.C. and Brownfield, M.S. (2013) Immunohistochemical localization of AT1a, AT1b, and AT2 angiotensin II receptor subtypes in the rat adrenal, pituitary, and brain with a perspective commentary. Int. J. Hypertens. 2013, 175428. – reference: 299) Frithiof, R., Xing, T., McKinley, M.J., May, C.N. and Ramchandra, R. (2014) Intracarotid hypertonic sodium chloride differentially modulates sympathetic nerve activity to the heart and kidney. Am. J. Physiol. Regul. Integr. Comp. Physiol. 306, R567–R575. – reference: 130) de Avila, C., Chometton, S., Lenglos, C., Calvez, J., Gundlach, A.L. and Timofeeva, E. (2018) Differential effects of relaxin-3 and a selective relaxin-3 receptor agonist on food and water intake and hypothalamic neuronal activity in rats. Behav. Brain Res. 336, 135–144. – reference: 98) Nomura, K., Hiyama, T.Y., Sakuta, H., Matsuda, T., Lin, C.H., Kobayashi, K. et al. (2019) [Na+] increases in body fluids sensed by central Nax induce sympathetically mediated blood pressure elevations via H+-dependent activation of ASIC1a. Neuron 101, 60–75.e66. – reference: 193) Heer, M., Baisch, F., Kropp, J., Gerzer, R. and Drummer, C. (2000) High dietary sodium chloride consumption may not induce body fluid retention in humans. Am. J. Physiol. Renal Physiol. 278, F585–F595. – reference: 228) Sequeira, S.M., Geerling, J.C. and Loewy, A.D. (2006) Local inputs to aldosterone-sensitive neurons of the nucleus tractus solitarius. Neuroscience 141, 1995–2005. – reference: 52) Mannari, T., Morita, S., Furube, E., Tominaga, M. and Miyata, S. (2013) Astrocytic TRPV1 ion channels detect blood-borne signals in the sensory circumventricular organs of adult mouse brains. Glia 61, 957–971. – reference: 56) Zaelzer, C., Hua, P., Prager-Khoutorsky, M., Ciura, S., Voisin, D.L., Liedtke, W. et al. (2015) ΔN-TRPV1: A molecular co-detector of body temperature and osmotic stress. Cell Rep. 13, 23–30. – reference: 154) Betley, J.N., Xu, S., Cao, Z.F.H., Gong, R., Magnus, C.J., Yu, Y. et al. (2015) Neurons for hunger and thirst transmit a negative-valence teaching signal. Nature 521, 180–185. – reference: 293) Adrogué, H.J. and Madias, N.E. (2007) Sodium and potassium in the pathogenesis of hypertension. N. Engl. J. Med. 356, 1966–1978. – reference: 80) Thrasher, T.N. and Keil, L.C. (1987) Regulation of drinking and vasopressin secretion: role of organum vasculosum laminae terminalis. Am. J. Physiol. 253, R108–R120. – reference: 295) Stocker, S.D., Monahan, K.D. and Browning, K.N. (2013) Neurogenic and sympathoexcitatory actions of NaCl in hypertension. Curr. Hypertens. Rep. 15, 538–546. – reference: 2) Park, R., Denton, D.A., McKinley, M.J., Pennington, G. and Weisinger, R.S. (1989) Intracerebroventricular saccharide infusions inhibit thirst induced by systemic hypertonicity. Brain Res. 493, 123–128. – reference: 74) Ramsay, D.J. and Thrasher, T.N. (1991) Regulation of fluid intake in dogs following water deprivation. Brain Res. Bull. 27, 495–499. – reference: 230) Geerling, J.C., Stein, M.K., Miller, R.L., Shin, J.W., Gray, P.A. and Loewy, A.D. (2011) FoxP2 expression defines dorsolateral pontine neurons activated by sodium deprivation. Brain Res. 1375, 19–27. – reference: 19) Matsumoto, M., Hiyama, T.Y., Kuboyama, K., Suzuki, R., Fujikawa, A. and Noda, M. (2015) Channel properties of Nax expressed in neurons. PLoS One 10, e0126109. – reference: 235) Lucas, L.R., Grillo, C.A. and McEwen, B.S. (2003) Involvement of mesolimbic structures in short-term sodium depletion: in situ hybridization and ligand-binding analyses. Neuroendocrinology 77, 406–415. – reference: 135) Olszewski, P.K., Klockars, A., Schioth, H.B. and Levine, A.S. (2010) Oxytocin as feeding inhibitor: maintaining homeostasis in consummatory behavior. Pharmacol. Biochem. Behav. 97, 47–54. – reference: 220) Fitts, D.A. and Masson, D.B. (1989) Forebrain sites of action for drinking and salt appetite to angiotensin or captopril. Behav. Neurosci. 103, 865–872. – reference: 282) Stricker, E.M. and Verbalis, J.G. (1987) Central inhibitory control of sodium appetite in rats: correlation with pituitary oxytocin secretion. Behav. Neurosci. 101, 560–567. – reference: 96) Matsuda, T., Hiyama, T.Y., Niimura, F., Matsusaka, T., Fukamizu, A., Kobayashi, K. et al. (2017) Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ. Nat. Neurosci. 20, 230–241. – reference: 298) Guyenet, P.G. (2006) The sympathetic control of blood pressure. Nat. Rev. Neurosci. 7, 335–346. – reference: 66) Tang, W., Strachan, R.T., Lefkowitz, R.J. and Rockman, H.A. (2014) Allosteric modulation of β-arrestin-biased angiotensin II type 1 receptor signaling by membrane stretch. J. Biol. Chem. 289, 28271–28283. – reference: 157) Gizowski, C., Zaelzer, C. and Bourque, C.W. (2016) Clock-driven vasopressin neurotransmission mediates anticipatory thirst prior to sleep. Nature 537, 685–688. – reference: 9) Andersson, B. (1977) Regulation of body fluids. Annu. Rev. Physiol. 39, 185–200. – reference: 108) Fitzsimons, J.T. and Simons, B.J. (1969) The effect on drinking in the rat of intravenous infusion of angiotensin, given alone or in combination with other stimuli of thirst. J. Physiol. 203, 45–57. – reference: 3) Denton, D.A., McKinley, M.J. and Weisinger, R.S. (1996) Hypothalamic integration of body fluid regulation. Proc. Natl. Acad. Sci. U.S.A. 93, 7397–7404. – reference: 6) Miyata, S. (2015) New aspects in fenestrated capillary and tissue dynamics in the sensory circumventricular organs of adult brains. Front. Neurosci. 9, 390. – reference: 266) Menani, J.V., Thunhorst, R.L. and Johnson, A.K. (1996) Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 270, R162–R168. – reference: 124) Lee, V.H., Lee, L.T., Chu, J.Y., Lam, I.P., Siu, F.K., Vaudry, H. et al. (2010) An indispensable role of secretin in mediating the osmoregulatory functions of angiotensin II. FASEB J. 24, 5024–5032. – reference: 300) Kawano, Y. and Ferrario, C.M. (1984) Neurohormonal characteristics of cardiovascular response due to intraventricular hypertonic NaCl. Am. J. Physiol. Heart Circ. Physiol. 247, H422–H428. – reference: 173) Tarjan, E., Denton, D.A. and Weisinger, R.S. (1988) Atrial natriuretic peptide inhibits water and sodium intake in rabbits. Regul. Pept. 23, 63–75. – reference: 196) Titze, J., Shakibaei, M., Schafflhuber, M., Schulze-Tanzil, G., Porst, M., Schwind, K.H. et al. (2004) Glycosaminoglycan polymerization may enable osmotically inactive Na+ storage in the skin. Am. J. Physiol. Heart Circ. Physiol. 287, H203–H208. – reference: 241) Eikemo, M., Løseth, G.E., Johnstone, T., Gjerstad, J., Willoch, F. and Leknes, S. (2016) Sweet taste pleasantness is modulated by morphine and naltrexone. Psychopharmacology (Berl) 233, 3711–3723. – reference: 314) Noda, M. (2007) Hydromineral neuroendocrinology: mechanism of sensing sodium levels in the mammalian brain. Exp. Physiol. 92, 513–522. – reference: 126) Hisaw, F.L. (1926) Experimental relaxation of the pubic ligament of the guinea pig. Proc. Soc. Exp. Biol. Med. 23, 661–663. – reference: 210) Geerling, J.C. and Loewy, A.D. (2006) Aldosterone-sensitive NTS neurons are inhibited by saline ingestion during chronic mineralocorticoid treatment. Brain Res. 1115, 54–64. – reference: 176) Zhu, B. and Herbert, J. (1996) Central antagonism of atrial natriuretic peptides on behavioral and hormonal responses to angiotensin II: mapping with c-fos. Brain Res. 734, 55–60. – reference: 151) Campos, C.A., Bowen, A.J., Schwartz, M.W. and Palmiter, R.D. (2016) Parabrachial CGRP neurons control meal termination. Cell Metab. 23, 811–820. – reference: 214) Jennings, J.H., Rizzi, G., Stamatakis, A.M., Ung, R.L. and Stuber, G.D. (2013) The inhibitory circuit architecture of the lateral hypothalamus orchestrates feeding. Science 341, 1517–1521. – reference: 110) Buggy, J. and Fisher, A.E. (1974) Evidence for a dual central role for angiotensin in water and sodium intake. Nature 250, 733–735. – reference: 136) Smith, C.M., Walker, L.L., Chua, B.E., McKinley, M.J., Gundlach, A.L., Denton, D.A. et al. (2015) Involvement of central relaxin-3 signalling in sodium (salt) appetite. Exp. Physiol. 100, 1064–1072. – reference: 260) Lança, A.J. and Van Der Kooy, D. (1985) A serotonin-containing pathway from the area postrema to the parabrachial nucleus in the rat. Neuroscience 14, 1117–1126. – reference: 163) Rosas-Arellano, M.P., Solano-Flores, L.P. and Ciriello, J. (1999) Co-localization of estrogen and angiotensin receptors within subfornical organ neurons. Brain Res. 837, 254–262. – reference: 219) Yamada, H. and Mendelsohn, F.A. (1989) Angiotensin II receptor binding in the rat hypothalamus and circumventricular organs during dietary sodium deprivation. Neuroendocrinology 50, 469–475. – reference: 296) Gavras, I. and Gavras, H. (2012) ‘Volume-expanded’ hypertension: the effect of fluid overload and the role of the sympathetic nervous system in salt-dependent hypertension. J. Hypertens. 30, 655–659. – reference: 234) Hubbell, C.L. and McCutcheon, N.B. (1993) Opioidergic manipulations affect intake of 3% NaCl in sodium-deficient rats. Pharmacol. Biochem. Behav. 46, 473–476. – reference: 204) Johnson, A.K. and Thunhorst, R.L. (1997) The neuroendocrinology of thirst and salt appetite: visceral sensory signals and mechanisms of central integration. Front. Neuroendocrinol. 18, 292–353. – reference: 290) Biondolillo, J.W., Williams, L.A. and King, M.S. (2009) Blocking glutamate receptors in the waist area of the parabrachial nucleus decreases taste reactivity behaviors in conscious rats. Chem. Senses 34, 221–230. – reference: 13) Weisinger, R.S., Considine, P., Denton, D.A., McKinley, M.J. and Mouw, D. (1979) Rapid effect of change in cerebrospinal fluid sodium concentration on salt appetite. Nature 280, 490–491. – reference: 89) Buggy, J. and Johnson, A.K. (1977) Preoptic-hypothalamic periventricular lesions: thirst deficits and hypernatremia. Am. J. Physiol. Regul. Integr. Comp. Physiol. 233, R44–R52. – reference: 112) Thunhorst, R.L., Ehrlich, K.J. and Simpson, J.B. (1990) Subfornical organ participates in salt appetite. Behav. Neurosci. 104, 637–642. – reference: 278) Oka, Y., Butnaru, M., von Buchholtz, L., Ryba, N.J. and Zuker, C.S. (2013) High salt recruits aversive taste pathways. Nature 494, 472–475. – reference: 44) Spassova, M.A., Hewavitharana, T., Xu, W., Soboloff, J. and Gill, D.L. (2006) A common mechanism underlies stretch activation and receptor activation of TRPC6 channels. Proc. Natl. Acad. Sci. U.S.A. 103, 16586–16591. – reference: 7) Kiecker, C. (2018) The origins of the circumventricular organs. J. Anat. 232, 540–553. – reference: 148) Kim, D.Y., Heo, G., Kim, M., Kim, H., Jin, J.A., Kim, H.K. et al. (2020) A neural circuit mechanism for mechanosensory feedback control of ingestion. Nature 580, 376–380. – reference: 253) Di Lorenzo, P.M. and Victor, J.D. (2003) Taste response variability and temporal coding in the nucleus of the solitary tract of the rat. J. Neurophysiol. 90, 1418–1431. – reference: 49) Ciura, S. and Bourque, C.W. (2006) Transient receptor potential vanilloid 1 is required for intrinsic osmoreception in organum vasculosum lamina terminalis neurons and for normal thirst responses to systemic hyperosmolality. J. Neurosci. 26, 9069–9075. – reference: 178) Buranarugsa, P. and Hubbard, J.I. (1988) Excitatory effects of atrial natriuretic peptide on rat subfornical organ neurons in vitro. Brain Res. Bull. 20, 627–631. – reference: 256) Franchini, L.F. and Vivas, L. (1999) Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis. Am. J. Physiol. Regul. Integr. Comp. Physiol. 276, R1180–R1187. – reference: 114) Matsusaka, T., Asano, T., Niimura, F., Kinomura, M., Shimizu, A., Shintani, A. et al. (2010) Angiotensin receptor blocker protection against podocyte-induced sclerosis is podocyte angiotensin II type 1 receptor-independent. Hypertension 55, 967–973. – reference: 270) Andrade, C.A.F., Barbosa, S.P., De Luca, L.A. and Menani, J.V. (2004) Activation of α2-adrenergic receptors into the lateral parabrachial nucleus enhances NaCl intake in rats. Neuroscience 129, 25–34. – reference: 227) Resch, J.M., Fenselau, H., Madara, J.C., Wu, C., Campbell, J.N., Lyubetskaya, A. et al. (2017) Aldosterone-sensing neurons in the NTS exhibit state-dependent pacemaker activity and drive sodium appetite via synergy with angiotensin II signaling. Neuron 96, 190–206.e197. – reference: 86) Lenkei, Z., Corvol, P. and Llorens-Cortes, C. (1995) The angiotensin receptor subtype AT1A predominates in rat forebrain areas involved in blood pressure, body fluid homeostasis and neuroendocrine control. Brain Res. Mol. Brain Res. 30, 53–60. – reference: 81) Anderson, J.W., Washburn, D.L.S. and Ferguson, A.V. (2000) Intrinsic osmosensitivity of subfornical organ neurons. Neuroscience 100, 539–547. – reference: 79) Mangiapane, M.L. and Simpson, J.B. (1980) Subfornical organ: forebrain site of pressor and dipsogenic action of angiotensin II. Am. J. Physiol. 239, R382–R389. – reference: 160) Tanaka, J., Kariya, K., Miyakubo, H., Sakamaki, K. and Nomura, M. (2002) Attenuated drinking response induced by angiotensinergic activation of subfornical organ projections to the paraventricular nucleus in estrogen-treated rats. Neurosci. Lett. 324, 242–246. – reference: 16) Watanabe, E., Hiyama, T.Y., Kodama, R. and Noda, M. (2002) Nax sodium channel is expressed in non-myelinating Schwann cells and alveolar type II cells in mice. Neurosci. Lett. 330, 109–113. – reference: 213) Jennings, J.H., Sparta, D.R., Stamatakis, A.M., Ung, R.L., Pleil, K.E., Kash, T.L. et al. (2013) Distinct extended amygdala circuits for divergent motivational states. Nature 496, 224–228. – reference: 170) Mietlicki, E.G., Nowak, E.L. and Daniels, D. (2009) The effect of ghrelin on water intake during dipsogenic conditions. Physiol. Behav. 96, 37–43. – reference: 205) Geerling, J.C. and Loewy, A.D. (2008) Central regulation of sodium appetite. Exp. Physiol. 93, 177–209. – reference: 99) Bellin, S.I., Bhatnagar, R.K. and Johnson, A.K. (1987) Periventricular noradrenergic systems are critical for angiotensin-induced drinking and blood pressure responses. Brain Res. 403, 105–112. – reference: 207) Ricardo, J.A. and Koh, E.T. (1978) Anatomical evidence of direct projections from the nucleus of the solitary tract to the hypothalamus, amygdala, and other forebrain structures in the rat. Brain Res. 153, 1–26. – reference: 22) Hori, S., Komatsu, Y., Shigemoto, R., Mizuno, N. and Nakanishi, S. (1992) Distinct tissue distribution and cellular localization of two messenger ribonucleic acids encoding different subtypes of rat endothelin receptors. Endocrinology 130, 1885–1895. – reference: 306) Diochot, S., Baron, A., Rash, L.D., Deval, E., Escoubas, P., Scarzello, S. et al. (2004) A new sea anemone peptide, APETx2, inhibits ASIC3, a major acid-sensitive channel in sensory neurons. EMBO J. 23, 1516–1525. – reference: 45) Bourque, C.W. (2008) Central mechanisms of osmosensation and systemic osmoregulation. Nat. Rev. Neurosci. 9, 519–531. – reference: 179) Ehrlich, K.J. and Fitts, D.A. (1990) Atrial natriuretic peptide in the subfornical organ reduces drinking induced by angiotensin or in response to water deprivation. Behav. Neurosci. 104, 365–372. – reference: 43) Clapham, D.E. (2003) TRP channels as cellular sensors. Nature 426, 517–524. – reference: 87) Barth, S.W. and Gerstberger, R. (1999) Differential regulation of angiotensinogen and AT1A receptor mRNA within the rat subfornical organ during dehydration. Brain Res. Mol. Brain Res. 64, 151–164. – reference: 37) Teruyama, R., Sakuraba, M., Wilson, L.L., Wandrey, N.E. and Armstrong, W.E. (2012) Epithelial Na+ sodium channels in magnocellular cells of the rat supraoptic and paraventricular nuclei. Am. J. Physiol. Endocrinol. Metab. 302, E273–E285. – reference: 166) Tschop, M., Smiley, D.L. and Heiman, M.L. (2000) Ghrelin induces adiposity in rodents. Nature 407, 908–913. – reference: 255) Yamamoto, T., Shimura, T., Sako, N., Sakai, N., Tanimizu, T. and Wakisaka, S. (1993) C-Fos expression in the parabrachial nucleus after ingestion of sodium chloride in the rat. Neuroreport 4, 1223–1226. – reference: 159) Levi, D.I., Wyrosdic, J.C., Hicks, A.I., Andrade, M.A., Toney, G.M., Prager-Khoutorsky, M. et al. (2021) High dietary salt amplifies osmoresponsiveness in vasopressin-releasing neurons. Cell Rep. 34, 108866. – reference: 191) Stricker, E.M., Thiels, E. and Verbalis, J.G. (1991) Sodium appetite in rats after prolonged dietary sodium deprivation: a sexually dimorphic phenomenon. Am. J. Physiol. 260, R1082–R1088. – reference: 261) Herbert, H., Moga, M.M. and Saper, C.B. (1990) Connections of the parabrachial nucleus with the nucleus of the solitary tract and the medullary reticular formation in the rat. J. Comp. Neurol. 293, 540–580. – reference: 186) Reis, L.C., Ramalho, M.J. and Antunes-Rodrigues, J. (1991) Participation of the median raphe nucleus and central serotoninergic pathways in the control of water electrolyte excretion. Braz. J. Med. Biol. Res. 24, 847–854. – reference: 251) Vaughan, C.W., Ingram, S.L., Connor, M.A. and Christie, M.J. (1997) How opioids inhibit GABA-mediated neurotransmission. Nature 390, 611–614. – reference: 243) Nogueiras, R., Romero-Picó, A., Vazquez, M.J., Novelle, M.G., López, M. and Diéguez, C. (2012) The opioid system and food intake: homeostatic and hedonic mechanisms. Obes. Facts 5, 196–207. – reference: 21) Watanabe, E., Hiyama, T.Y., Shimizu, H., Kodama, R., Hayashi, N., Miyata, S. et al. (2006) Sodium-level-sensitive sodium channel Nax is expressed in glial laminate processes in the sensory circumventricular organs. Am. J. Physiol. Regul. Integr. Comp. Physiol. 290, R568–R576. – reference: 32) Arena, E.A., Longo, W.E., Roberts, K.E., Geibel, P., Nateqi, J., Brandstetter, M. et al. (2012) Functional role of NHE4 as a pH regulator in rat and human colonic crypts. Am. J. Physiol. Cell Physiol. 302, C412–C418. – reference: 50) Hollis, J.H., McKinley, M.J., D’Souza, M., Kampe, J. and Oldfield, B.J. (2008) The trajectory of sensory pathways from the lamina terminalis to the insular and cingulate cortex: a neuroanatomical framework for the generation of thirst. Am. J. Physiol. Regul. Integr. Comp. Physiol. 294, R1390–R1401. – reference: 132) Albert-Gasco, H., Ma, S., Ros-Bernal, F., Sanchez-Perez, A.M., Gundlach, A.L. and Olucha-Bordonau, F.E. (2017) GABAergic neurons in the rat medial septal complex express relaxin-3 receptor (RXFP3) mRNA. Front. Neuroanat. 11, 133. – reference: 88) Sakuta, H., Lin, C.-H., Yamada, M., Kita, Y., Tokuoka, S.M., Shimizu, T. et al. (2020) Nax-positive glial cells in the organum vasculosum laminae terminalis produce epoxyeicosatrienoic acids to induce water intake in response to increases in [Na+] in body fluids. Neurosci. Res. 154, 45–51. – reference: 69) Saltmarsh, M. (2001) Thirst: or, why do people drink? Nutr. Bull. 26, 53–58. – reference: 127) Hudson, P., Haley, J., John, M., Cronk, M., Crawford, R., Haralambidis, J. et al. (1983) Structure of a genomic clone encoding biologically active human relaxin. Nature 301, 628–631. – reference: 245) Zardetto-Smith, A.M., Beltz, T.G. and Johnson, A.K. (1994) Role of the central nucleus of the amygdala and bed nucleus of the stria terminalis in experimentally-induced salt appetite. Brain Res. 645, 123–134. – reference: 30) Sakuta, H., Lin, C.H., Hiyama, T.Y., Matsuda, T., Yamaguchi, K., Shigenobu, S. et al. (2020) SLC9A4 in the organum vasculosum of the lamina terminalis is a [Na+] sensor for the control of water intake. Pflugers Arch. 472, 609–624. – reference: 31) Bookstein, C., Musch, M.W., DePaoli, A., Xie, Y., Rabenau, K., Villereal, M. et al. (1996) Characterization of the rat Na+/H+ exchanger isoform NHE4 and localization in rat hippocampus. Am. J. Physiol. 271, C1629–C1638. – reference: 38) Chandrashekar, J., Kuhn, C., Oka, Y., Yarmolinsky, D.A., Hummler, E., Ryba, N.J.P. et al. (2010) The cells and peripheral representation of sodium taste in mice. Nature 464, 297–301. – reference: 11) Fitzsimons, J.T. (1989) Bengt Andersson’s pioneering demonstration of the hypothalamic “drinking area” and the subsequent osmoreceptor/sodium receptor controversy. Acta Physiol. Scand. Suppl. 583, 15–25. – reference: 181) Antunes-Rodrigues, J., McCann, S.M. and Samson, W.K. (1986) Central administration of atrial natriuretic factor inhibits saline preference in the rat. Endocrinology 118, 1726–1728. – reference: 311) Shirai, Y., Miura, K., Nakamura-Utsunomiya, A., Ishizuka, K., Hattori, M. and Hattori, M. (2021) Analysis of water and electrolyte imbalance in a patient with adipsic hypernatremia associated with subfornical organ-targeting antibody. CEN Case Reports. – reference: 250) Chieng, B.C.H., Christie, M.J. and Osborne, P.B. (2006) Characterization of neurons in the rat central nucleus of the amygdala: Cellular physiology, morphology, and opioid sensitivity. J. Comp. Neurol. 497, 910–927. – reference: 109) Epstein, A.N., Fitzsimons, J.T. and Rolls, B.J. (1970) Drinking induced by injection of angiotensin into the rain of the rat. J. Physiol. 210, 457–474. – reference: 156) Zimmerman, C.A., Lin, Y.C., Leib, D.E., Guo, L., Huey, E.L., Daly, G.E. et al. (2016) Thirst neurons anticipate the homeostatic consequences of eating and drinking. Nature 537, 680–684. – reference: 242) Kelley, A.E., Bakshi, V.P., Haber, S.N., Steininger, T.L., Will, M.J. and Zhang, M. (2002) Opioid modulation of taste hedonics within the ventral striatum. Physiol. Behav. 76, 365–377. – reference: 72) Adrogué, H.J. and Madias, N.E. (2000) Hyponatremia. N. Engl. J. Med. 342, 1581–1589. – reference: 280) Stricker, E.M. and Verbalis, J.G. (1996) Central inhibition of salt appetite by oxytocin in rats. Regul. Pept. 66, 83–85. – reference: 194) Titze, J., Maillet, A., Lang, R., Gunga, H.C., Johannes, B., Gauquelin-Koch, G. et al. (2002) Long-term sodium balance in humans in a terrestrial space station simulation study. Am. J. Kidney Dis. 40, 508–516. – reference: 101) Hall, J.E. (2003) Historical perspective of the renin-angiotensin system. Mol. Biotechnol. 24, 27–39. – reference: 150) Carter, M.E., Soden, M.E., Zweifel, L.S. and Palmiter, R.D. (2013) Genetic identification of a neural circuit that suppresses appetite. Nature 503, 111–114. – reference: 310) Hiyama, T.Y., Utsunomiya, A.N., Matsumoto, M., Fujikawa, A., Lin, C.H., Hara, K. et al. (2017) Adipsic hypernatremia without hypothalamic lesions accompanied by autoantibodies to subfornical organ. Brain Pathol. 27, 323–331. – reference: 85) el Ghissassi, M., Thornton, S.N. and Nicolaïdis, S. (1995) Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis. Am. J. Physiol. 268, R1401–R1405. – reference: 104) Weisinger, R.S., Blair-West, J.R., Burns, P., Denton, D.A., McKinley, M.J. and Tarjan, E. (1996) The role of angiotensin II in ingestive behaviour: a brief review of angiotensin II, thirst and Na appetite. Regul. Pept. 66, 73–81. – reference: 303) Nicol, C.J., Adachi, M., Akiyama, T.E. and Gonzalez, F.J. (2005) PPARγ in endothelial cells influences high fat diet-induced hypertension. Am. J. Hypertens. 18, 549–556. – reference: 41) Borgnia, M., Nielsen, S., Engel, A. and Agre, P. (1999) Cellular and molecular biology of the aquaporin water channels. Annu. Rev. Biochem. 68, 425–458. – reference: 198) Richter, C.P. (1936) Increased salt appetite in adrenalectomized rats. Am. J. Physiol. Leg. Cont. 115, 155–161. – reference: 279) Gimpl, G. and Fahrenholz, F. (2001) The oxytocin receptor system: structure, function, and regulation. Physiol. Rev. 81, 629–683. – reference: 291) Group, I.C.R. (1988) Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ 297, 319. – reference: 59) Sakuta, H., Nishihara, E., Hiyama, T.Y., Lin, C.H. and Noda, M. (2016) Nax signaling evoked by an increase in [Na+] in CSF induces water intake via EET-mediated TRPV4 activation. Am. J. Physiol. Regul. Integr. Comp. Physiol. 311, R299–R306. – reference: 55) Sharif Naeini, R., Witty, M.F., Séguéla, P. and Bourque, C.W. (2006) An N-terminal variant of Trpv1 channel is required for osmosensory transduction. Nat. Neurosci. 9, 93–98. – reference: 100) Deschepper, C.F. (1994) Angiotensinogen: hormonal regulation and relative importance in the generation of angiotensin II. Kidney Int. 46, 1561–1563. – reference: 107) Johnson, A.K. and Schwob, J.E. (1975) Cephalic angiotensin receptors mediating drinking to systemic angiotensin II. Pharmacol. Biochem. Behav. 3, 1077–1084. – reference: 18) Noda, M. and Hiyama, T.Y. (2005) Sodium-level-sensitive Sodium Channel and Salt-Intake Behavior. Chem. Senses 30, i44–i45. – reference: 117) Oka, Y., Ye, M. and Zuker, C.S. (2015) Thirst driving and suppressing signals encoded by distinct neural populations in the brain. Nature 520, 349–352. – reference: 28) Orlowski, J. and Grinstein, S. (2011) Na+/H+ exchangers. Compr. Physiol. 2011, 2083–2100. – reference: 189) Bojesen, E. (1966) Concentrations of aldosterone and corticosterone in peripheral plasma of rats. The effects of salt depletion, salt repletion, potassium loading and intravenous injections of renin and angiotensin II. Eur. J. Steroids 1, 145–169. – reference: 238) De Oliveira, L.B., De Luca, L.A. and Menani, J.V. (2008) Opioid activation in the lateral parabrachial nucleus induces hypertonic sodium intake. Neuroscience 155, 350–358. – reference: 289) Miller, R.L., Stein, M.K. and Loewy, A.D. (2011) Serotonergic inputs to FoxP2 neurons of the pre-locus coeruleus and parabrachial nuclei that project to the ventral tegmental area. Neuroscience 193, 229–240. – reference: 17) Hiyama, T.Y., Watanabe, E., Ono, K., Inenaga, K., Tamkun, M.M., Yoshida, S. et al. (2002) Nax channel involved in CNS sodium-level sensing. Nat. Neurosci. 5, 511–512. – reference: 175) Nakamura, M., Katsuura, G., Nakao, K. and Imura, H. (1985) Antidipsogenic action of α-human atrial natriuretic polypeptide administered intracerebroventricularly in rats. Neurosci. Lett. 58, 1–6. – reference: 277) Heck, G.L., Mierson, S. and DeSimone, J.A. (1984) Salt taste transduction occurs through an amiloride-sensitive sodium transport pathway. Science 223, 403–405. – reference: 48) Strotmann, R., Harteneck, C., Nunnenmacher, K., Schultz, G. and Plant, T.D. (2000) OTRPC4, a nonselective cation channel that confers sensitivity to extracellular osmolarity. Nat. Cell Biol. 2, 695–702. – reference: 60) Yang, F., Zhou, L., Wang, D., Yang, L.L., Yuan, G.R. and Huang, Q.Y. (2016) Suppression of TRPV4 channels ameliorates anti-dipsogenic effects under hypoxia in the subfornical organ of rats. Sci. Rep. 6, 30168. – reference: 174) Itoh, H., Nakao, K., Yamada, T., Shirakami, G., Kangawa, K., Minamimo, N. et al. (1988) Antidipsogenic action of a novel peptide, ‘brain natriuretic peptide’, in rats. Eur. J. Pharmacol. 150, 193–196. – reference: 203) de Kloet, A.D., Liu, M., Rodríguez, V., Krause, E.G. and Sumners, C. (2015) Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control. Am. J. Physiol. Regul. Integr. Comp. Physiol. 309, R444–R458. – reference: 134) McKinley, M.J., Mathai, M.L., McAllen, R.M., McClear, R.C., Miselis, R.R., Pennington, G.L. et al. (2004) Vasopressin secretion: osmotic and hormonal regulation by the lamina terminalis. J. Neuroendocrinol. 16, 340–347. – reference: 68) Lefkowitz, R.J. (1998) G protein-coupled receptors: III. New roles for receptor kinases and β-arrestins in receptor signaling and desensitization. J. Biol. Chem. 273, 18677–18680. – reference: 111) Fitts, D.A. and Masson, D.B. (1990) Preoptic angiotensin and salt appetite. Behav. Neurosci. 104, 643–650. – reference: 222) Edwards, G.L. and Ritter, R.C. (1982) Area postrema lesions increase drinking to angiotensin and extracellular dehydration. Physiol. Behav. 29, 943–947. – reference: 77) Ichiki, T., Augustine, V. and Oka, Y. (2019) Neural populations for maintaining body fluid balance. Curr. Opin. Neurobiol. 57, 134–140. – reference: 122) Chu, J.Y.S., Lee, L.T.O., Lai, C.H., Vaudry, H., Chan, Y.S., Yung, W.H. et al. (2009) Secretin as a neurohypophysial factor regulating body water homeostasis. Proc. Natl. Acad. Sci. U.S.A. 106, 15961–15966. – reference: 133) Ma, S., Smith, C.M., Blasiak, A. and Gundlach, A.L. (2017) Distribution, physiology and pharmacology of relaxin-3/RXFP3 systems in brain. Br. J. Pharmacol. 174, 1034–1048. – reference: 95) Kinsman, B.J., Simmonds, S.S., Browning, K.N., Wenner, M.M., Farquhar, W.B. and Stocker, S.D. (2020) Integration of hypernatremia and angiotensin II by the organum vasculosum of the lamina terminalis regulates thirst. J. Neurosci. 40, 2069. – reference: 62) Mizuno, A., Matsumoto, N., Imai, M. and Suzuki, M. (2003) Impaired osmotic sensation in mice lacking TRPV4. Am. J. Physiol. Cell Physiol. 285, C96–C101. – reference: 84) Pool, A.H., Wang, T., Stafford, D.A., Chance, R.K., Lee, S., Ngai, J. et al. (2020) The cellular basis of distinct thirst modalities. Nature 588, 112–117. – reference: 29) Verma, V., Bali, A., Singh, N. and Jaggi, A.S. (2015) Implications of sodium hydrogen exchangers in various brain diseases. J. Basic Clin. Physiol. Pharmacol. 26, 417–426. – reference: 192) Wolf, G. and Stricker, E.M. (1967) Sodium appetite elicited by hypovolemia in adrenalectomized rats: Reevaluation of the “reservoir” hypothesis. J. Comp. Physiol. Psychol. 63, 252–257. – reference: 121) Bai, J.J., Tan, C.D. and Chow, B.K.C. (2016) Secretin, at the hub of water-salt homeostasis. Am. J. Physiol. Renal Physiol. 312, F852–F860. – reference: 169) Pulman, K.J., Fry, W.M., Cottrell, G.T. and Ferguson, A.V. (2006) The subfornical organ: a central target for circulating feeding signals. J. Neurosci. 26, 2022–2030. – reference: 281) Puryear, R., Rigatto, K.V., Amico, J.A. and Morris, M. (2001) Enhanced salt intake in oxytocin deficient mice. Exp. Neurol. 171, 323–328. – reference: 27) Shimizu, H., Watanabe, E., Hiyama, T.Y., Nagakura, A., Fujikawa, A., Okado, H. et al. (2007) Glial Nax channels control lactate signaling to neurons for brain [Na+] sensing. Neuron 54, 59–72. – reference: 143) Augustine, V., Gokce, S.K., Lee, S., Wang, B., Davidson, T.J., Reimann, F. et al. (2018) Hierarchical neural architecture underlying thirst regulation. Nature 555, 204–209. – reference: 33) Bookstein, C., Musch, M.W., DePaoli, A., Xie, Y., Villereal, M., Rao, M.C. et al. (1994) A unique sodium-hydrogen exchange isoform (NHE-4) of the inner medulla of the rat kidney is induced by hyperosmolarity. J. Biol. Chem. 269, 29704–29709. – reference: 40) Ramsay, D.J., Thrasher, T.N. and Keil, L.C. (1983) The organum vasculosum laminae terminalis: a critical area for osmoreception. Prog. Brain Res. 60, 91–98. – reference: 229) Stein, M.K. and Loewy, A.D. (2010) Area postrema projects to FoxP2 neurons of the pre-locus coeruleus and parabrachial nuclei: brainstem sites implicated in sodium appetite regulation. Brain Res. 1359, 116–127. – reference: 244) Galaverna, O., De Luca, L.A., Schulkin, J., Yao, S.-Z. and Epstein, A.N. (1992) Deficits in NaCl ingestion after damage to the central nucleus of the amygdala in the rat. Brain Res. Bull. 28, 89–98. – reference: 162) Tanaka, J., Miyakubo, H., Fujisawa, S. and Nomura, M. (2003) Reduced dipsogenic response induced by angiotensin II activation of subfornical organ projections to the median preoptic nucleus in estrogen-treated rats. Exp. Neurol. 179, 83–89. – reference: 301) Ribeiro, N., Panizza Hdo, N., Santos, K.M., Ferreira-Neto, H.C. and Antunes, V.R. (2015) Salt-induced sympathoexcitation involves vasopressin V1a receptor activation in the paraventricular nucleus of the hypothalamus. Am. J. Physiol. Regul. Integr. Comp. Physiol. 309, R1369–R1379. – reference: 91) Johnson, R.F., Beltz, T.G., Thunhorst, R.L. and Johnson, A.K. (2003) Investigations on the physiological controls of water and saline intake in C57BL/6 mice. Am. J. Physiol. Regul. Integr. Comp. Physiol. 285, R394–R403. – reference: 152) Gong, R., Xu, S., Hermundstad, A., Yu, Y. and Sternson, S.M. (2020) Hindbrain double-negative feedback mediates palatability-guided food and water consumption. Cell 182, 1589–1605.e1522. – reference: 259) Fulwiler, C.E. and Saper, C.B. (1984) Subnuclear organization of the efferent connections of the parabrachial nucleus in the rat. Brain Res. Rev. 7, 229–259. – reference: 297) Henderson, K.K. and Byron, K.L. (2007) Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways. J. Appl. Physiol. 102, 1402–1409. – reference: 140) Zimmerman, C.A., Huey, E.L., Ahn, J.S., Beutler, L.R., Tan, C.L., Kosar, S. et al. (2019) A gut-to-brain signal of fluid osmolarity controls thirst satiation. Nature 568, 98–102. – reference: 183) Antunes-Rodrigues, J., Machado, B.H., Andrade, H.A., Mauad, H., Ramalho, M.J., Reis, L.C. et al. (1992) Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion. Proc. Natl. Acad. Sci. U.S.A. 89, 6828. – reference: 283) Katoh, A., Fujihara, H., Ohbuchi, T., Onaka, T., Hashimoto, T., Kawata, M. et al. (2011) Highly visible expression of an oxytocin-monomeric red fluorescent protein 1 fusion gene in the hypothalamus and posterior pituitary of transgenic rats. Endocrinology 152, 2768–2774. – reference: 180) Hattori, Y., Kasai, M., Uesugi, S., Kawata, M. and Yamashita, H. (1988) Atrial natriuretic polypeptide depresses angiotensin II induced excitation of neurons in the rat subfornical organ in vitro. Brain Res. 443, 355–359. – reference: 199) Sakai, R.R., Nicolaidis, S. and Epstein, A.N. (1986) Salt appetite is suppressed by interference with angiotensin II and aldosterone. Am. J. Physiol. Regul. Integr. Comp. Physiol. 251, R762–R768. – reference: 92) Lind, R.W., Thunhorst, R.L. and Johnson, A.K. (1984) The subfornical organ and the integration of multiple factors in thirst. Physiol. Behav. 32, 69–74. – reference: 61) Ciura, S., Prager-Khoutorsky, M., Thirouin, Z.S., Wyrosdic, J.C., Olson, J.E., Liedtke, W. et al. (2018) Trpv4 mediates hypotonic inhibition of central osmosensory neurons via taurine gliotransmission. Cell Rep. 23, 2245–2253. – reference: 177) Weisinger, R.S., Blair-West, J.R., Denton, D.A. and Tarjan, E. (1992) Central administration of atrial natriuretic peptide suppresses sodium and water intake of sheep. Brain Res. 579, 113–118. – reference: 10) Andersson, B. (1971) Thirst—and brain control of water balance. Am. Sci. 59, 408–415. – reference: 267) Menani, J.V. and Johnson, A.K. (1998) Cholecystokinin actions in the parabrachial nucleus: Effects on thirst and salt appetite. Am. J. Physiol. Regul. Integr. Comp. Physiol. 275, R1431–R1437. – reference: 285) Castro, L., Athanazio, R., Barbetta, M., Ramos, A.C., Angelo, A.L., Campos, I. et al. (2003) Central 5-HT2B/2C and 5-HT3 receptor stimulation decreases salt intake in sodium-depleted rats. Brain Res. 981, 151–159. – reference: 24) Hiyama, T.Y., Yoshida, M., Matsumoto, M., Suzuki, R., Matsuda, T., Watanabe, E. et al. (2013) Endothelin-3 expression in the subfornical organ enhances the sensitivity of Nax, the brain sodium-level sensor, to suppress salt intake. Cell Metab. 17, 507–519. – reference: 4) McKinley, M.J., McAllen, R.M., Davern, P., Giles, M.E., Penschow, J., Sunn, N. et al. (2003) The sensory circumventricular organs of the mammalian brain. Adv. Anat. Embryol. Cell Biol. 172, III–XII, 1–122, back cover. – reference: 200) Fluharty, S.J. and Epstein, A.N. (1983) Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: II. Synergistic interaction with systemic mineralocorticoids. Behav. Neurosci. 97, 746–758. – reference: 209) Geerling, J.C., Engeland, W.C., Kawata, M. and Loewy, A.D. (2006) Aldosterone target neurons in the nucleus tractus solitarius drive sodium appetite. J. Neurosci. 26, 411–417. – reference: 184) Bosler, O. and Descarries, L. (1988) Monoamine innervation of the organum vasculosum laminae terminalis (OVLT): a high resolution radioautographic study in the rat. J. Comp. Neurol. 272, 545–561. – reference: 292) Mente, A., O’Donnell, M.J., Rangarajan, S., McQueen, M.J., Poirier, P., Wielgosz, A. et al. (2014) Association of urinary sodium and potassium excretion with blood pressure. N. Engl. J. Med. 371, 601–611. – reference: 312) Saker, P., Carey, S., Grohmann, M., Farrell, M.J., Ryan, P.J., Egan, G.F. et al. (2020) Regional brain responses associated with using imagination to evoke and satiate thirst. Proc. Natl. Acad. Sci. U.S.A. 117, 13750–13756. – reference: 1) Cox, P.S., Denton, D.A., Mouw, D.R. and Tarjan, E. (1987) Natriuresis induced by localized perfusion within the third cerebral ventricle of sheep. Am. J. Physiol. 252, R1–R6. – reference: 218) Mendelsohn, F.A., Quirion, R., Saavedra, J.M., Aguilera, G. and Catt, K.J. (1984) Autoradiographic localization of angiotensin II receptors in rat brain. Proc. Natl. Acad. Sci. U.S.A. 81, 1575–1579. – reference: 231) Shin, J.W., Geerling, J.C., Stein, M.K., Miller, R.L. and Loewy, A.D. (2011) FoxP2 brainstem neurons project to sodium appetite regulatory sites. J. Chem. Neuroanat. 42, 1–23. – reference: 308) Burke, P.G., Abbott, S.B., Coates, M.B., Viar, K.E., Stornetta, R.L. and Guyenet, P.G. (2014) Optogenetic stimulation of adrenergic C1 neurons causes sleep state-dependent cardiorespiratory stimulation and arousal with sighs in rats. Am. J. Respir. Crit. Care Med. 190, 1301–1310. – reference: 271) Andrade, C.A.F., De Luca, L.A., Colombari, D.S.A. and Menani, J.V. (2006) Alpha2-adrenergic activation in the lateral parabrachial nucleus induces NaCl intake under conditions of systemic hyperosmolarity. Neuroscience 142, 21–28. – reference: 215) Sandhu, E.C., Fernando, A.B.P., Irvine, E.E., Tossell, K., Kokkinou, M., Glegola, J. et al. (2018) Phasic stimulation of midbrain dopamine neuron activity reduces salt consumption. eNeuro 5, ENEURO.0064-18.2018. – reference: 240) Smith, C.M., Walker, L.L., Leeboonngam, T., McKinley, M.J., Denton, D.A. and Lawrence, A.J. (2016) Endogenous central amygdala mu-opioid receptor signaling promotes sodium appetite in mice. Proc. Natl. Acad. Sci. U.S.A. 113, 13893–13898. – reference: 78) Noda, M. and Sakuta, H. (2013) Central regulation of body-fluid homeostasis. Trends Neurosci. 36, 661–673. – reference: 202) Coble, J.P., Grobe, J.L., Johnson, A.K. and Sigmund, C.D. (2015) Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ. Am. J. Physiol. Regul. Integr. Comp. Physiol. 308, R238–R249. – reference: 39) Lin, W., Finger, T.E., Rossier, B.C. and Kinnamon, S.C. (1999) Epithelial Na+ channel subunits in rat taste cells: localization and regulation by aldosterone. J. Comp. Neurol. 405, 406–420. – reference: 307) Bohlen, C.J., Chesler, A.T., Sharif-Naeini, R., Medzihradszky, K.F., Zhou, S., King, D. et al. (2011) A heteromeric Texas coral snake toxin targets acid-sensing ion channels to produce pain. Nature 479, 410–414. – ident: 159 doi: 10.1016/j.celrep.2021.108866 – ident: 262 doi: 10.1016/0361-9230(93)90054-F – ident: 265 doi: 10.1152/ajpregu.1995.269.5.R1044 – ident: 308 doi: 10.1164/rccm.201407-1262OC – ident: 200 doi: 10.1037/0735-7044.97.5.746 – ident: 179 doi: 10.1037/0735-7044.104.2.365 – ident: 1 doi: 10.1152/ajpregu.1987.252.1.R1 – ident: 254 doi: 10.1016/0304-3940(93)90609-O – ident: 92 doi: 10.1016/0031-9384(84)90072-6 – ident: 107 doi: 10.1016/0091-3057(75)90020-9 – ident: 98 doi: 10.1016/j.neuron.2018.11.017 – ident: 79 doi: 10.1152/ajpregu.1980.239.5.R382 – ident: 18 doi: 10.1093/chemse/bjh105 – ident: 124 doi: 10.1096/fj.10-165399 – ident: 27 doi: 10.1016/j.neuron.2007.03.014 – ident: 37 doi: 10.1152/ajpendo.00407.2011 – ident: 235 doi: 10.1159/000071312 – ident: 28 doi: 10.1002/cphy.c110020 – ident: 129 doi: 10.1016/j.peptides.2010.02.020 – ident: 6 doi: 10.3389/fnins.2015.00390 – ident: 194 doi: 10.1053/ajkd.2002.34908 – ident: 297 doi: 10.1152/japplphysiol.00825.2006 – ident: 141 doi: 10.1016/j.neuron.2019.04.039 – ident: 96 doi: 10.1038/nn.4463 – ident: 76 doi: 10.1038/nrn.2017.71 – ident: 195 doi: 10.1152/ajprenal.00200.2003 – ident: 110 doi: 10.1038/250733a0 – ident: 125 doi: 10.1096/fj.13-246868 – ident: 186 – ident: 268 doi: 10.1152/ajpregu.00311.2001 – ident: 47 doi: 10.1016/S0092-8674(00)00143-4 – ident: 99 doi: 10.1016/0006-8993(87)90128-4 – ident: 60 doi: 10.1038/srep30168 – ident: 177 doi: 10.1016/0006-8993(92)90749-Y – ident: 4 doi: 10.1007/978-3-642-55532-9_1 – ident: 78 doi: 10.1016/j.tins.2013.08.004 – ident: 298 doi: 10.1038/nrn1902 – ident: 59 doi: 10.1152/ajpregu.00352.2015 – ident: 119 doi: 10.1126/science.aav3932 – ident: 204 doi: 10.1006/frne.1997.0153 – ident: 63 doi: 10.1038/emboj.2008.233 – ident: 101 doi: 10.1385/MB:24:1:27 – ident: 142 doi: 10.1016/j.cell.2019.11.040 – ident: 57 doi: 10.1152/ajpregu.00102.2014 – ident: 313 doi: 10.1038/s41593-021-00850-4 – ident: 10 – ident: 55 doi: 10.1038/nn1614 – ident: 257 doi: 10.1016/B978-0-08-027337-2.50045-6 – ident: 271 doi: 10.1016/j.neuroscience.2006.04.015 – ident: 136 doi: 10.1113/EP085349 – ident: 64 doi: 10.1038/ncb1137 – ident: 252 doi: 10.1016/j.brainres.2010.03.055 – ident: 44 doi: 10.1073/pnas.0606894103 – ident: 123 doi: 10.1385/MN:26:1:097 – ident: 134 doi: 10.1111/j.0953-8194.2004.01184.x – ident: 36 doi: 10.1152/ajpregu.00063.2005 – ident: 221 doi: 10.1016/0006-8993(81)90707-1 – ident: 261 doi: 10.1002/cne.902930404 – ident: 8 doi: 10.1186/1824-7288-36-78 – ident: 157 doi: 10.1038/nature19756 – ident: 118 doi: 10.1113/JP274667 – ident: 303 doi: 10.1016/j.amjhyper.2004.10.032 – ident: 169 doi: 10.1523/JNEUROSCI.3218-05.2006 – ident: 280 doi: 10.1016/0167-0115(96)00058-4 – ident: 258 doi: 10.1016/0006-8993(84)90140-9 – ident: 185 doi: 10.1016/0028-3908(87)90118-3 – ident: 275 doi: 10.1016/j.brainres.2010.11.075 – ident: 106 doi: 10.1016/j.cmet.2010.09.011 – ident: 256 doi: 10.1152/ajpregu.1999.276.4.R1180 – ident: 244 doi: 10.1016/0361-9230(92)90234-O – ident: 219 doi: 10.1159/000125265 – ident: 287 doi: 10.1016/S0006-8993(98)00530-7 – ident: 197 doi: 10.1111/apha.13006 – ident: 245 doi: 10.1016/0006-8993(94)91645-4 – ident: 71 doi: 10.1056/NEJM200005183422006 – ident: 127 doi: 10.1038/301628a0 – ident: 237 doi: 10.1007/s00213-001-0932-y – ident: 162 doi: 10.1006/exnr.2002.8054 – ident: 247 doi: 10.1016/j.neuroscience.2012.07.068 – ident: 281 doi: 10.1006/exnr.2001.7776 – ident: 163 doi: 10.1016/S0006-8993(99)01672-8 – ident: 89 doi: 10.1152/ajpregu.1977.233.1.R44 – ident: 206 doi: 10.1046/j.1365-2826.2003.00969.x – ident: 216 doi: 10.1073/pnas.1834556100 – ident: 95 doi: 10.1523/JNEUROSCI.2208-19.2020 – ident: 103 doi: 10.1016/0091-3057(76)90248-3 – ident: 146 doi: 10.3389/fphys.2014.00436 – ident: 264 doi: 10.1111/j.1365-2826.1992.tb00194.x – ident: 199 doi: 10.1152/ajpregu.1986.251.4.R762 – ident: 180 doi: 10.1016/0006-8993(88)91633-2 – ident: 207 doi: 10.1016/0006-8993(78)91125-3 – ident: 238 doi: 10.1016/j.neuroscience.2008.06.011 – ident: 52 doi: 10.1002/glia.22488 – ident: 120 doi: 10.1113/jphysiol.1902.sp000920 – ident: 240 doi: 10.1073/pnas.1616664113 – ident: 158 doi: 10.1016/j.neuron.2016.11.021 – ident: 232 doi: 10.1038/s41586-019-1053-2 – ident: 284 doi: 10.1016/0079-6107(93)90009-9 – ident: 34 doi: 10.1152/ajpcell.1997.272.1.C90 – ident: 167 doi: 10.1210/jcem.86.12.8111 – ident: 172 doi: 10.1016/0361-9230(85)90044-9 – ident: 224 doi: 10.1002/cne.20993 – ident: 234 doi: 10.1016/0091-3057(93)90382-4 – ident: 31 doi: 10.1152/ajpcell.1996.271.5.C1629 – ident: 282 doi: 10.1037/0735-7044.101.4.560 – ident: 306 doi: 10.1038/sj.emboj.7600177 – ident: 156 doi: 10.1038/nature18950 – ident: 168 doi: 10.1016/j.neuroscience.2013.09.008 – ident: 173 doi: 10.1016/0167-0115(88)90422-3 – ident: 228 doi: 10.1016/j.neuroscience.2006.05.059 – ident: 104 doi: 10.1016/0167-0115(96)00052-3 – ident: 133 doi: 10.1111/bph.13659 – ident: 213 doi: 10.1038/nature12041 – ident: 115 doi: 10.1016/j.neuron.2017.11.041 – ident: 263 doi: 10.1016/0361-9230(95)02084-5 – ident: 279 doi: 10.1152/physrev.2001.81.2.629 – ident: 49 doi: 10.1523/JNEUROSCI.0877-06.2006 – ident: 45 doi: 10.1038/nrn2400 – ident: 58 doi: 10.1152/ajpregu.00003.2008 – ident: 294 doi: 10.1111/j.1523-1755.2004.66018.x – ident: 148 doi: 10.1038/s41586-020-2167-2 – ident: 296 doi: 10.1097/HJH.0b013e32834f6de1 – ident: 149 doi: 10.1038/s41593-017-0014-z – ident: 203 doi: 10.1152/ajpregu.00078.2015 – ident: 35 doi: 10.1152/ajpregu.00242.2013 – ident: 53 doi: 10.1002/cphy.c120001 – ident: 161 doi: 10.1016/S0031-9384(03)00095-7 – ident: 174 doi: 10.1016/0014-2999(88)90769-8 – ident: 176 doi: 10.1016/S0006-8993(96)00615-4 – ident: 220 doi: 10.1037/h0092457 – start-page: 1223 issn: 0959-4965 year: 1993 ident: 255 publication-title: Neuroreport doi: 10.1097/00001756-199309000-00003 – ident: 300 doi: 10.1152/ajpheart.1984.247.3.H422 – ident: 218 doi: 10.1073/pnas.81.5.1575 – ident: 193 doi: 10.1152/ajprenal.2000.278.4.F585 – ident: 20 doi: 10.1523/JNEUROSCI.2795-04.2004 – ident: 24 doi: 10.1016/j.cmet.2013.02.018 – ident: 202 doi: 10.1152/ajpregu.00486.2014 – ident: 42 doi: 10.1016/S0092-8674(02)00670-0 – ident: 188 doi: 10.1016/S0140-6736(01)36734-X – ident: 61 doi: 10.1016/j.celrep.2018.04.090 – ident: 93 doi: 10.1038/nature01807 – ident: 248 doi: 10.1016/j.neuroscience.2012.12.026 – ident: 192 doi: 10.1037/h0024357 – ident: 277 doi: 10.1126/science.6691151 – ident: 43 doi: 10.1038/nature02196 – ident: 210 doi: 10.1016/j.brainres.2006.07.091 – ident: 50 doi: 10.1152/ajpregu.00869.2007 – ident: 73 doi: 10.1016/j.cub.2016.11.019 – ident: 260 doi: 10.1016/0306-4522(85)90281-7 – ident: 77 doi: 10.1016/j.conb.2019.01.014 – ident: 114 doi: 10.1161/HYPERTENSIONAHA.109.141994 – ident: 126 doi: 10.3181/00379727-23-3107 – ident: 314 doi: 10.1113/expphysiol.2006.035659 – ident: 94 doi: 10.1152/physrev.00021.2001 – ident: 249 doi: 10.1016/j.neuroscience.2005.02.004 – ident: 40 doi: 10.1016/S0079-6123(08)64377-0 – ident: 289 doi: 10.1016/j.neuroscience.2011.07.008 – ident: 54 doi: 10.1523/JNEUROSCI.0237-05.2005 – ident: 152 doi: 10.1016/j.cell.2020.07.031 – ident: 276 doi: 10.1016/j.neulet.2003.12.040 – ident: 113 doi: 10.1016/0006-8993(90)90245-7 – ident: 187 doi: 10.1073/pnas.91.25.12022 – ident: 117 doi: 10.1038/nature14108 – ident: 102 doi: 10.1152/physrev.00036.2005 – start-page: 908 issn: 0028-0836 year: 2000 ident: 166 publication-title: ?Nature doi: 10.1038/35038090 – ident: 223 doi: 10.1016/0006-8993(96)00277-6 – ident: 305 doi: 10.1074/jbc.M003643200 – ident: 311 doi: 10.1007/s13730-021-00638-2 – ident: 12 doi: 10.1016/0006-8993(78)90619-4 – ident: 90 doi: 10.1037/h0077759 – ident: 155 doi: 10.1126/science.aan6747 – ident: 227 doi: 10.1016/j.neuron.2017.09.014 – ident: 153 doi: 10.1073/pnas.2009233117 – ident: 205 doi: 10.1113/expphysiol.2007.039891 – ident: 39 doi: 10.1002/(SICI)1096-9861(19990315)405:3<406::AID-CNE10>3.0.CO;2-F – ident: 278 doi: 10.1038/nature11905 – ident: 70 doi: 10.1152/physrev.1998.78.3.583 – ident: 184 doi: 10.1002/cne.902720408 – ident: 29 doi: 10.1515/jbcpp-2014-0117 – ident: 208 doi: 10.1016/0006-8993(94)01453-O – ident: 229 doi: 10.1016/j.brainres.2010.08.085 – ident: 231 doi: 10.1016/j.jchemneu.2011.05.003 – ident: 143 doi: 10.1038/nature25488 – ident: 310 doi: 10.1111/bpa.12409 – ident: 91 doi: 10.1152/ajpregu.00130.2003 – ident: 105 doi: 10.1155/2013/175428 – ident: 236 doi: 10.1159/000102536 – ident: 144 doi: 10.1210/jendso/bvab048.1052 – ident: 135 doi: 10.1016/j.pbb.2010.05.026 – ident: 290 doi: 10.1093/chemse/bjn081 – ident: 191 doi: 10.1152/ajpregu.1991.260.6.R1082 – ident: 48 doi: 10.1038/35036318 – ident: 46 doi: 10.1371/journal.pone.0022246 – ident: 253 doi: 10.1152/jn.00177.2003 – ident: 62 doi: 10.1152/ajpcell.00559.2002 – ident: 14 doi: 10.1016/S0896-6273(00)00116-1 – ident: 72 doi: 10.1056/NEJM200005253422107 – ident: 183 doi: 10.1073/pnas.89.15.6828 – ident: 222 doi: 10.1016/0031-9384(82)90348-1 – ident: 16 doi: 10.1016/S0304-3940(02)00708-5 – ident: 66 doi: 10.1074/jbc.M114.585067 – ident: 67 doi: 10.1002/jcb.26552 – ident: 80 doi: 10.1152/ajpregu.1987.253.1.R108 – start-page: 1726 issn: 0013-7227 year: 1986 ident: 181 publication-title: Endocrinology doi: 10.1210/endo-118-4-1726 – ident: 274 doi: 10.1016/j.neuroscience.2011.02.019 – ident: 3 doi: 10.1073/pnas.93.14.7397 – ident: 19 doi: 10.1371/journal.pone.0126109 – ident: 283 doi: 10.1210/en.2011-0006 – ident: 26 doi: 10.1152/ajpcell.00601.2001 – ident: 32 doi: 10.1152/ajpcell.00163.2011 – ident: 84 doi: 10.1038/s41586-020-2821-8 – ident: 211 doi: 10.1152/ajpregu.00391.2006 – ident: 189 – ident: 5 doi: 10.1096/fasebj.7.8.8500693 – ident: 269 doi: 10.1016/S0306-4522(03)00316-6 – ident: 7 doi: 10.1111/joa.12771 – ident: 85 doi: 10.1152/ajpregu.1995.268.6.R1401 – ident: 307 doi: 10.1038/477410a – ident: 302 doi: 10.1016/j.neuron.2014.12.048 – ident: 38 doi: 10.1038/nature08783 – ident: 182 doi: 10.1073/pnas.88.7.2956 – ident: 295 doi: 10.1007/s11906-013-0385-9 – ident: 83 doi: 10.1126/science.181.4105.1172 – ident: 122 doi: 10.1073/pnas.0903695106 – ident: 292 doi: 10.1056/NEJMoa1311989 – ident: 74 doi: 10.1016/0361-9230(91)90148-D – ident: 304 doi: 10.1161/HYPERTENSIONAHA.115.05936 – ident: 69 doi: 10.1046/j.1467-3010.2001.00097.x – ident: 100 doi: 10.1038/ki.1994.446 – ident: 242 doi: 10.1016/S0031-9384(02)00751-5 – ident: 65 doi: 10.1126/scisignal.2000769 – ident: 259 doi: 10.1016/0165-0173(84)90012-2 – ident: 81 doi: 10.1016/S0306-4522(00)00313-4 – ident: 154 doi: 10.1038/nature14416 – ident: 312 doi: 10.1073/pnas.2002825117 – ident: 160 doi: 10.1016/S0304-3940(02)00203-3 – ident: 121 doi: 10.1152/ajprenal.00191.2015 – ident: 250 doi: 10.1002/cne.21025 – ident: 291 doi: 10.1136/bmj.297.6644.319 – ident: 112 doi: 10.1037/0735-7044.104.4.637 – ident: 196 doi: 10.1152/ajpheart.01237.2003 – ident: 309 doi: 10.1016/j.neuron.2010.04.017 – ident: 13 doi: 10.1038/280490a0 – ident: 25 doi: 10.1038/bjp.2008.92 – ident: 230 doi: 10.1016/j.brainres.2010.11.028 – ident: 132 doi: 10.3389/fnana.2017.00133 – ident: 131 doi: 10.1002/cne.22442 – ident: 273 doi: 10.1016/j.neuroscience.2009.08.048 – ident: 190 doi: 10.1016/S0031-9384(75)80032-1 – ident: 243 doi: 10.1159/000338163 – ident: 139 doi: 10.1006/mcne.1993.1018 – ident: 56 doi: 10.1016/j.celrep.2015.08.061 – ident: 87 doi: 10.1016/S0169-328X(98)00308-8 – ident: 23 doi: 10.1152/ajpregu.90560.2008 – ident: 212 doi: 10.1152/ajpheart.00515.2002 – ident: 217 doi: 10.1113/expphysiol.2008.044446 – ident: 170 doi: 10.1016/j.physbeh.2008.08.004 – ident: 138 doi: 10.1038/s41467-020-19191-0 – ident: 88 doi: 10.1016/j.neures.2019.05.006 – ident: 108 doi: 10.1113/jphysiol.1969.sp008848 – ident: 246 doi: 10.3138/9781487578466-018 – ident: 175 doi: 10.1016/0304-3940(85)90319-2 – ident: 239 doi: 10.1016/j.bbr.2015.03.047 – ident: 22 doi: 10.1210/en.130.4.1885 – ident: 285 doi: 10.1016/S0006-8993(03)03015-4 – ident: 9 doi: 10.1146/annurev.ph.39.030177.001153 – ident: 109 doi: 10.1113/jphysiol.1970.sp009220 – ident: 270 doi: 10.1016/j.neuroscience.2004.07.042 – ident: 116 doi: 10.1016/j.neuron.2011.05.028 – ident: 164 doi: 10.1152/ajpregu.00222.2013 – ident: 233 doi: 10.1007/s11064-017-2336-3 – ident: 33 doi: 10.1016/S0021-9258(18)43937-3 – ident: 137 doi: 10.1016/0167-0115(84)90011-9 – ident: 215 doi: 10.1523/ENEURO.0064-18.2018 – ident: 82 doi: 10.1007/s00424-014-1662-4 – ident: 178 doi: 10.1016/0361-9230(88)90223-7 – ident: 209 doi: 10.1523/JNEUROSCI.3115-05.2006 – ident: 201 doi: 10.1016/0196-9781(82)90113-9 – ident: 198 doi: 10.1152/ajplegacy.1936.115.1.155 – ident: 151 doi: 10.1016/j.cmet.2016.04.006 – ident: 51 doi: 10.1073/pnas.1735416100 – ident: 130 doi: 10.1016/j.bbr.2017.08.044 – ident: 41 doi: 10.1146/annurev.biochem.68.1.425 – ident: 267 doi: 10.1152/ajpregu.1998.275.5.R1431 – ident: 251 doi: 10.1038/37610 – ident: 140 doi: 10.1038/s41586-019-1066-x – ident: 165 doi: 10.1038/45230 – ident: 97 doi: 10.1152/ajpregu.1980.238.5.R372 – ident: 128 doi: 10.1210/endo-107-3-691 – ident: 30 doi: 10.1007/s00424-020-02389-y – ident: 150 doi: 10.1038/nature12596 – ident: 2 doi: 10.1016/0006-8993(89)91006-8 – ident: 171 doi: 10.1073/pnas.82.24.8720 – ident: 21 doi: 10.1152/ajpregu.00618.2005 – ident: 75 doi: 10.1152/nips.01470.2003 – ident: 293 doi: 10.1056/NEJMra064486 – ident: 214 doi: 10.1126/science.1241812 – ident: 147 doi: 10.1152/ajpregu.00251.2012 – ident: 11 – ident: 266 doi: 10.1152/ajpregu.1996.270.1.R162 – ident: 225 doi: 10.1161/CIRCULATIONAHA.115.019341 – ident: 226 doi: 10.1038/nn.4451 – ident: 286 doi: 10.1590/S0001-37652004000100008 – ident: 86 doi: 10.1016/0169-328X(94)00272-G – ident: 241 doi: 10.1007/s00213-016-4403-x – ident: 301 doi: 10.1152/ajpregu.00312.2015 – ident: 15 doi: 10.1523/JNEUROSCI.20-20-07743.2000 – ident: 68 doi: 10.1074/jbc.273.30.18677 – ident: 145 doi: 10.1038/nn.4575 – ident: 111 doi: 10.1037/0735-7044.104.4.643 – ident: 272 doi: 10.1016/j.brainres.2009.08.094 – ident: 288 doi: 10.1038/s41593-019-0573-2 – ident: 299 doi: 10.1152/ajpregu.00460.2013 – ident: 17 doi: 10.1038/nn0602-856 |
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SubjectTerms | [Na+] sensor Aldosterone Angiotensin Angiotensin II Blood pressure body fluid homeostasis Body fluids Brain Cerebrospinal fluid Electrolytes Homeostasis Hormones Hypertension Hypotonicity Kidneys Osmoregulation osmosensor Physiology Review Rodents Salt salt appetite Sensors thirst Trauma Vasopressin |
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Title | Central regulation of body fluid homeostasis |
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