Renin release after hemorrhage and after suprarenal aortic constriction in dogs without sodium delivery to the macula densa.

To study the possible factors that control renin secretion by the kidney, a model has been developed to prevent glomerular filtration in the dog. Ureteral ligaton was combined with a 2-hour period of total renal ischemia to induce tubular degeneration and cessation of glomerular filtration. After the surgical procedures, the dogs were maintained for 4 days by peritoneal dialysis. The absence of lissamine green dye in the renal tubules after an intra-aortic injection provided evidence that filtration had ceased. Plasma renin activity was significantly increased in six conscious dogs at 30, 60, and 90 minutes after hemorrhage of 20 ml/kg body weight. In another group of five conscious animals, suprarenal aortic constriction produced increases in plasma renin activity at 30, 60, and 90 minutes that were 3 to 4 times the control values before aortic constriction. Plasma renin substrate concentration did not change significantly after hemorrhage or after aortic constriction. In a third group of five dogs, only the left kidney was subjected to ureteral ligation and renal ischemia. These dogs were anesthetized and renal blood flow was measured with an electromagnetic flowmeter. After hemorrhage (20 ml/kg), renin secretion increased significantly above control levels at 30, 45, and 60 minutes. It is concluded that sodium delivery to the macula densa is not essential for renin secretion. ADDITIONAL