Endogenous Angiotensin and Sodium Appetite
Intracerebroventricular administration of angiotensin II or its precursors causes an increase in sodium appetite that is independent of the thirst also aroused by these substances. After renin, increased intakes of water and NaCl persist for many hours, sometimes for days, owing to continuing generation of angiotensin II from locally available components of the cerebral reninangiotensin system1. The initial increase in sodium appetite is not secondary to sodium loss2, though angiotensin also causes natriuresis, because the animals may develop a substantial positive sodium balance. Nor is the increased NaCl intake the consequence of the accompanying increase in water intake since it still occurs when access to water is prevented. The appetite is specific for the sodium ion. A pre-existing hypovolaemia (Fuller & Fitzsimons, this workshop), or treatment with mineralocorticoids3 augments the effect of angiotensin on sodium appetite.
KeywordsAngiotensin Converting Enzyme Inhibitor Renin Secretion Increase Water Intake Sodium Appetite Ureteric Ligation
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