Mechanisms regulating renin release in dogs with thoracic caval constriction.

Abstract

In dogs with chronic thoracic caval constriction, renal denervation was followed by a fall in plasma renin activity from an average of 82.1 ± 1.5 (SE) ng angiotensin/ml of plasma over a 9-day control period to 40.8 ± 2.3 ng/ml for a 13-day period after denervation ( P < 0.001); normal value was 4.7 ± 0.7 ng/ml. There was no detectable effect of renal denervation on the marked sodium retention. Thus the renal nerves contributed to the high plasma renin activity during caval constriction, but renal innervation was not essential for hypersecretion of renin. In a second group of dogs with caval constriction, the nonfiltering kidney model with a nonfunctional macula densa was produced, and renin secretion was measured before and after papaverine infusion into the left renal artery. Papaverine decreased renin secretion from 1090 ± 185 ng angiotensin/min to 497 ± 140 ng/min ( P < 0.005). This initial rate of renin secretion of 1090 ng/min was higher than that from a nonfiltering left kidney of 190 ± 50 ng/min in otherwise normal dogs ( P < 0.001). In a third series of dogs with caval constriction but with filtering kidneys, papaverine produced a similar decrease in renin secretion and an associated increase in sodium excretion. Since papaverine dilated the renal arterioles and the macula densa was nonfunctional in dogs with a nonfiltering kidney, these data support the concept that an intrarenal vascular receptor mediates the elevation in renin secretion in this model with chronic ascites. The striking decrease in renin secretion in response to intrarenal propranolol in dogs with either a filtering or a nonfiltering kidney indicates that a beta receptor is also involved.