Control of Renin Secretion

Abstract

Renin secretion was found to be controlled by a renal baroreceptor rather than by ischemia. Development of a sensitive assay technique that detects renin in small quantities of renal venous and peripheral arterial plasma has permitted the demonstration that the rate of renin secretion varies inversely with the level of arterial pressure independently of renal blood flow. When mean renal perfusion pressure was reduced 5 to 40 mm Hg by a constricting band around the aorta above the level of the renal arteries, increased renin secretion commenced within 60 seeonds. Reductions of this magnitude did not necessarily cause mean perfusion pressure to fall below control levels of diastolic perfusion pressure. Rises in perfusion pressure had the reverse effect, reducing the rate of renin secretion again without measurable change in renal blood flow. Compression of the kidney within an oncometer by an applied forece of from 15 to 40 mm Hg also caused increases in the rate of renin secretion in the absence of change in total renal blood flow. Reduction of pulse pressure alone did not provoke secretion of renin, nor did reduced oxygen tension, or renal ischemia. Rise in perfusion pressure due to occlusion of the common carotid arteries was associated with reduction in the rate of renin secretion. A small amount of renin was secreted continuously under the conditions of these experiments; physiologic changes in mean perfusion pressure served to alter the rate. This suggests that a renal baroreceptor mechanism regulates renin secretion under normal circumstances and that arterial pressure tends to stabilize at a level at which renin secretion is minimal.