The renin—angiotensin system in drinking and cardiovascular responses to isoprenaline in the rat

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Abstract
The role of the renin-angiotensin [A] system in isoprenaline-induced drinking was studied in the rat. Captopril, an inhibitor of A-converting enzyme, was used to block the synthesis of AII either in the circulation alone or in the brain as well. S.c. injections of isoprenaline (0.1 mg/kg) alone caused 9 rats to drink 8.4 .+-. 0.9 ml water in 3 h. Pretreatment with doses of captopril (0.1-1.0 mg/kg, s.c.), which inhibit conversion of AI to AII in the circulation but not in the brain, dose-dependently enhanced the drinking response to isoprenaline. Captopril alone did not cause drinking. Higher doses of captopril (5.0-100 mg/kg, s.c.), which inhibit conversion of AI to AII in the brain and in the blood, caused dose-dependent inhibition of drinking elicited by isoprenaline. The highest dose of captopril tested (100 mg/kg, s.c.) completely blocked the drinking response to isoprenaline (0.1 or 0.33 mg/kg, s.c.) for at least 45 min. This inhibition was not caused by general debility of the rats; animals deprived of water (12 h) and treated with captopril and isoprenaline drank as much as water-deprived controls. No evidence was found that blocking the renin-A system inhibits drinking because it exacerbates isoprenaline-induced hypotension. After injection of isoprenaline the mean arterial pressure of nephrectomized rats or rats pretreated with the high dose (100 mg/kg, s.c.) of captopril (which blocked drinking) was only slightly lower (5-10 mm Hg) than that of rats pretreated with the low dose (0.5 mg/kg, s.c.) of captopril (which enhanced drinking). Water deprivation, which caused rats treated with isoprenaline and captopril to drink, did not increase arterial pressure. Pitressin increased the arterial pressure of rats treated with isoprenaline and captopril but did not cause drinking. The renin-A system has a direct and essential role in the drinking response to isoprenaline.

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