with Graded Stimulation by Aortic Constriction Evidence for a Renal Vascular Mechanism in Renin Release: New Observations

To examine the possibility of a renal intravascular receptor for renin secretion, bilateral ureteral ligation and a two-hour period of renal ischemia were used to produce a nonfiltering kidney model in dogs. In conscious animals with both innervated and denervated, nonfiltering kidneys, hemorrhage and suprarenal aortic constriction produced significant increases in plasma renin activity. To measure renin secretion directly, a unilateral, nonfiltering kidney was produced, and renal blood flow was determined with a square-wave electromagnetic flowmeter in anesthetized dogs. Renin secretion was significantly elevated after a 20 ml/kg hemorrhage in these animals. In another group of dogs, adrenalectomy was combined with renal denervation in the unilateral, nonfiltering kidney model. In these animals hemorrhage produced significant increases in renin secretion. After a recovery period three of these dogs were subjected to graded constriction of the suprarenal aorta. Slight decreases in blood pressure with and without decreases in renal blood flow produced increases in renin secretion. Since increased renin secretion occurred in the absence of sodium delivery to the macula densa, from denervated kidneys, and without the major portion of circulating catecholatnines, it is suggested that an intrinsic receptor for renin release is present within the renal vascular tree.