Effect of an angiotensin antagonist, Sar1-Ala8-angiotensin II on physiological thirst.

Initially it was shown that infusion of Sar1-Ala8-angiotensin II (P113) into the third ventricle (50-100 mug/ml at 1.1 ml/hr) effectively abolished the large water intake induced 1-2 min after beginning an intracarotid infusion of angiotensin II at 800 ng/min which causes an unphysiologically high concentration of angiotensin II in cerebral arterial blood. Infusion of P113 (50-100 mug/ml at 1.1 ml/hr) into the third brain ventricle for 20 min prior to and during presentation of water to sheep after 48 hr water deprivation did not reduce water intake. Water intake associated with rapid food intake or carotid artery infusion of hypertonic NaC1 was similarly unaffected by intraventricular administration of P113. While high concentrations of angiotensin II are dipsogenic in sheep, these results cast doubt on a contributory role for angiotensin II in thirst caused by water depletion or rapid food intake in the sheep.