Roles of brain angiotensins II and III in thirst and sodium appetite

The current study examined the effects of intracerebroventricular (icv) infused aminopeptidase-resistant analogs of angiotensin II (AngII) and angiotensin III (AngIII) on thirst and sodium appetite. The analogs, [D-Asp 1D-Arg 2]AngII and [D-Arg 1]AngIII, were further protected from degradation by pr...

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Published inBrain research Vol. 1060; no. 1; pp. 108 - 117
Main Authors Wilson, Wendy L., Roques, Bernard P., Llorens-Cortes, Catherine, Speth, Robert C., Harding, Joseph W., Wright, John W.
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 26.10.2005
Amsterdam Elsevier
New York, NY
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Summary:The current study examined the effects of intracerebroventricular (icv) infused aminopeptidase-resistant analogs of angiotensin II (AngII) and angiotensin III (AngIII) on thirst and sodium appetite. The analogs, [D-Asp 1D-Arg 2]AngII and [D-Arg 1]AngIII, were further protected from degradation by pretreatment with the aminopeptidase A inhibitor, EC33, or the aminopeptidase N inhibitor, PC18. Prior to icv infusions, rats were sodium depleted with furosemide, followed by the angiotensin-converting enzyme inhibitor captopril, to block endogenous angiotensin formation. Both angiotensin analogs, at either of the two doses, were capable of eliciting fluid intakes of water and 0.3 M NaCl. Water and saline intakes were increased to a similar extent by 125 and 1250 pmol of [D-Asp 1D-Arg 2]AngII. [D-Arg 1]AngIII produced a dose-dependent increase in water intake, whereas saline intake was equivalently increased by the 125 and 1250 pmol infusions. Pretreatment with EC33 or PC18 decreased water and saline intakes in response to [D-Asp 1D-Arg 2]AngII, while pretreatment with PC18 altered the time course of the [D-Arg 1]AngIII-induced water and saline intakes. The ability of both inhibitors to decrease, but not completely block, AngII analog-induced intakes, coupled with the altered time course of the responses induced by the AngIII analog in the presence of PC18, supports the hypothesis that both AngII and AngIII are active ligands in brain angiotensin-mediated thirst and sodium appetite. However, these results do not resolve the primary question of whether conversion of AngII to AngIII is a prerequisite to dipsogenic and salt appetite responses in the brain.
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ISSN:0006-8993
1872-6240
0006-8993
DOI:10.1016/j.brainres.2005.08.032