Intrarenal renin-angiotensin-sodium interdependent mechanism controlling postclamp renal artery pressure and renin release in the conscious dog with chronic one-kidney Goldblatt hypertension.

Abstract

We studied postclamp renal artery pressure and renin release in eight conscious dogs with one-kidney Goldblatt hypertension. On normal sodium intake, intrarenal blockade of angiotensin II with Sar1-Ala8-angiotension II (P-113, saralasin acetate) markedly decreased postclamp renal artery pressure and increased renin release during the first 5 days after renal artery constriction. We found that 10-14 days after renal artery constriction, the maintenance of postclamp renal artery pressure and negative feedback on renin release became markedly less dependent on angiotensin II, as shown by almost no change in postclamp renal pressure or renin release with intrarenal blockade of angiotensin II. At this stage of our study the dogs were given a sodium diet of less than 5 mEq/day and we found that within 5-10 days intrarenal blockade of angiotensin II once again markedly decreased postclamp renal artery pressure and increased renin release. These observations support the concept of an angiotensin II-sodium interdependent negative feedback mechanism for renin release.