Centrally Produced Nitric Oxide And The Regulation Of Body Fluid And Blood Pressure Homeostases

SUMMARY 1. Nitric oxide (NO) tonically inhibits the basal release of vasopressin and oxytocin into plasma. 2. Nitric oxide inhibition on vasopressin secretion is removed, while that on oxytocin is enhanced, during water deprivation, hypovolaemia, moderate osmotic stimulation and angiotensin (Ang)II....

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Published inClinical and experimental pharmacology & physiology Vol. 27; no. 5-6; pp. 450 - 459
Main Authors Kadekaro, Massako, Summy-Long, Joan Y
Format Journal Article
LanguageEnglish
Published Melbourne, Australia Blackwell Science Pty 01.05.2000
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Summary:SUMMARY 1. Nitric oxide (NO) tonically inhibits the basal release of vasopressin and oxytocin into plasma. 2. Nitric oxide inhibition on vasopressin secretion is removed, while that on oxytocin is enhanced, during water deprivation, hypovolaemia, moderate osmotic stimulation and angiotensin (Ang)II. This results in a preferential release of vasopressin over oxytocin that promotes conservation of water. 3. Nitric oxide facilitates drinking behaviour stimulated by water deprivation, osmotic stimulation, haemorrhage and AngII. Together with the hormonal response, NO produces a positive water balance during reductions in intracellular and intravascular volumes. 4. Nitric oxide produced within the central nervous system maintains resting arterial blood pressure partially by attenuating the pressor actions of AngII and prostaglandins. 5. Central production of NO is enhanced during osmotic stimulation to counterbalance the salt‐induced pressor response. 6. Paradoxically, central production of NO is also enhanced during haemorrhage, presumably to maintain peripheral vasodilation and blood flow to vital organs.
Bibliography:ark:/67375/WNG-6W069MJH-H
ArticleID:CEP3264
istex:4D14582D0F225D5C8E9A234F9C53F045D0C1E2AA
Paper based on presentation at the meeting Role of Circumventricular Organs: Gateways to the Brain for Humoral Influences Subserving Homeostasis, Daintree Rainforest, Australia, September 1997. This paper has been peer reviewed.
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ISSN:0305-1870
1440-1681
DOI:10.1046/j.1440-1681.2000.03264.x