Salt appetite is suppressed by interference with angiotensin II and aldosterone.
Blockade of central but not peripheral mineralocorticoid receptors, with the antimineralocorticoid RU-28318, reduces but does not suppress salt appetite aroused by sodium depletion in the rat. When central mineralocorticoid blockade is combined with captopril treatment to prevent formation of endogenous angiotensin II the appetite is completely suppressed. Suppression of the appetite occurred without changes in the animals' spontaneous ingestive behaviors, sodium excretion, or insulin-induced food intake. These results demonstrate that a synergy of angiotensin II and aldosterone is responsible for the expression of depletion-induced salt appetite in the rat.
D000450:Aldosterone / Q000502:physiology*; D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000502:physiology*; D000818:Animals; D001066:Appetite / Q000187:drug effects / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D002552:Cerebral Ventricles / Q000502:physiology; D007328:Insulin / Q000494:pharmacology; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride; D013148:Spironolactone / Q000031:analogs & derivatives / Q000494:pharmacology
D007328:Insulin; D000804:Angiotensin II; D013148:Spironolactone; D012965:Sodium Chloride; D000450:Aldosterone; C041006:RU 28318; D002216:Captopril