Renal mechanisms for suppression of renin secretion by atrial natriuretic factor

Abstract

The effects of synthetic atrial natriuretic factor on renin secretion were examined in anesthetized dogs with either a single filtering kidney or a single denervated nonfiltering kidney. In dogs with a single filtering kidney (Series 1, n = 6), a priming dose of atrial natriuretic factor (2 μg/kg, i.v.) followed by sustained intravenous infusions at doses of 200 and 400 ng/kg/min for 20 minutes each produced striking decrements (p < 0.05) in renin secretion, from 1083 ± 322 to 205 ± 120 and 286 ± 168 ng of angiotensin I per minute. This fall in renin secretion was associated with significant increases (p < 0.05) in creatinine clearance, urine flow, sodium excretion, and the filtered load of sodium. Renal blood flow increased only transiently. In dogs with a single denervated nonfiltering kidney (Series 2, n = 6), infusion of atrial natriuretic factor at these doses also produced marked inhibition (p < 0.05) of renin secretion, from 311 ± 98 to 72 ± 22 and 91 ± 37 ng of angiotensin I per minute. Renal blood flow remained significantly elevated (p < 0.05) throughout the infusion, in contrast to renal blood flow in Series I, Similar results were obtained in a third series of dogs (n = 6) with a single denervated nonfiltering kidney, during sustained intrarenal arterial infusions of atrial natriuretic factor. These results suggest that an increase in the sodium load delivered to the macula densa is not essential for the inhibition of renin secretion by atrial natriuretic factor. We conclude that suppression of renin secretion by atrial natriuretic factor is mediated through its interactions with the two intrarenal receptor mechanisms, the renal vascular receptor and the macula densa. It is also possible that atrial natriuretic factor has a direct inhibitory action on the juxtaglomerular cells. © 1986 American Heart Association, Inc.