Sodium appetite during captopril blockade of endogenous angiotensin II formation

Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. In addition, they may act synergistically to arouse a sodium appetite. If so, then blockade of endogenous angiotensin should decrease the appetite. In experiments reported here, captopril (SQ 14,225) was given peripherally to rats to block conversion of angiotensin I to angiotensin II. It both enhanced and suppressed sodium depletion-induced sodium appetite. The appetite was suppressed when captopril was given in high doses, which block conversion centrally as well as peripherally. The same doses of captopril had no effect on urinary sodium excretion or on sodium appetite aroused by mineralocorticoid treatment. Low doses, which block conversion only in the periphery, enhanced salt intake elicited by depletion, and the enhancement was abolished by captopril given directly into the brain. Therefore the enhancement was probably due to a captopril-induced increase of peripheral angiotensin I, which gained access to the brain and was converted there to angiotensin II.