Isoproterenol-induced thirst: renal and extrarenal mechanisms.

When given systemically, isoproterenol will induce water intake in various species. The drug also causes hypotension and renin release from the kidney. Angiotensin II and arterial baroreceptors have been hypothesized to be involved in the mediation of beta-adrenoceptor agonist-induced thirst, but their relative importance has been disputed. In the present series of experiments, isoproterenol was infused intravenously at different rates into nephrectomized and ureteric-ligated rats. Thus, different levels of hypotension could be achieved and maintained while water intake was measured. Also, plasma levels of angiotensin II were determined in ureteric-ligated rats following the intravenous infusion of a dipsogenic dose of isoproterenol. The results indicate that for moderate blood pressure changes a renal-related factor, probably angiotensin II, plays a major role in the mediation of isoproterenol-induced thirst. Under extreme conditions involving a very dramatic drop of arterial blood pressure, extrarenal mechanisms (e.g., arterial baroreceptors) are implicated.