Angiotensin does contribute to drinking induced by caval ligation in rat

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Abstract
In small (0.5 mg/kg) s.c. doses, the angiotensin-converting enzyme inhibitor, captopril, greatly enhanced drinking in response to caval ligation in the rat. Drinking was not secondary to urinary water loss since the rats developed a substantial positive fluid balance. High (50 mg/kg) s.c. doses of captopril reduced drinking to a level below that following caval ligation alone. This effect could be mimicked by giving repeated intracerebroventricular injections of captopril (total amount 110 .mu.g) to rats treated with the lower s.c. dose of captopril. With this combination, not only did the lower dose enhancement disappear, but the basal caval ligation drinking response was also reduced with a total dose of captopril of < 2% of the higher s.c. dose alone. When conversion of angiotensin I to angiotensin II is prevented in the brain as well as systemically, drinking in response to caval ligation is reduced although not entirely prevented. Drinking is multifactorial, depending on angiotensin as well as nonangiotensin mechanisms.