Pressor action of intravenous angiotensin II reduces drinking response in rats.

We investigated whether the pressor response to intravenous angiotensin II (ANG II) suppresses drinking. All experiments were done on conscious water-replete rats (200-400 g) with chronic vascular cannulas. Two rates of ANG II infusion (16.7 and 100 ng/min for 90 min) were tested; captopril (0.33 mg/min) was infused simultaneously to prevent endogenous production of ANG II. Both doses of ANG II increased mean arterial pressure (MAP) by 40-50 mmHg for the duration of the infusions, but water intakes were small. The drinking response was increased as much as fivefold, however, when the pressor response was reduced by injecting either isoproterenol (0.01 or 0.1 mg/kg, sc), diazoxide (20, 30, or 75 mg/kg, sc), or minoxidil (10 mg/kg, ip) 15 min after starting the ANG II infusion. The closer MAP was returned to normal, the greater was the drinking response. Since lowering MAP also reduced urinary water losses, net fluid intake increased even more dramatically. It is unlikely that the vasodilators directly stimulated thirst in the experiments because the dose of captopril used completely blocked drinking to these agents given alone. A situation of high circulating levels of ANG II but with MAP near or below normal more closely resembles physiological conditions of dehydration. Our results demonstrate that intravenous ANG II is a very potent dipsogen under these conditions.