In order to assess the role of angiotensin in the genesis of certain types of thirst, rats were administered the angiotensin converting enzyme inhibitor, captopril, in an attempt to block the increased water intake induced either by water deprivation or by i.p. administration of hypertonic saline. Water deprivation for 24 hr resulted in an increased water intake. Acute administration of 50 mg of captopril per kg i.p. at 45 or 60, but not at 15 or 30, min before return of water to the dehydrated rats significantly attenuated the drinking response. Rats administered 1% b.wt. i.p. of 0.25, 0.50, 0.75 or 1.00 M NaCl solution increased proportionately their water intake. Acute administration of 35 mg of captopril per kg b. wt. i.p. 15 min before loading with NaCl solution at any of the above concentrations had no effect on the increased thirst induced. These findings suggest that hypertonic saline-induced thirst is not mediated by angiotensin II receptors while water deprivation-induced thirst may involve both osmoreceptors and angiotensin II receptors.