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We determined the effects of </-propranolol and renal denervation on furosemide-induced renin release in the anesthetized dog. rf-Propranolol possesses only membrane-stabilizing properties, whereas the /-isomer produces beta adrenergic blockade. To separate the vascular and macula densa mechanisms of the juxtaglomerular apparatus effectively, nonfiltering kidneys were produced by combining 2.5 hours of renal ischemia with ureteral ligation. In some dogs, renal denervation was accomplished by relocating the nonfiltering kidney into the neck during the 2.5-hour ischemic interval. Administration of d-propranolol in a priming dose of 1 mg/kg, iv, followed by an intravenous infusion of 1 mg/kg per hour decreased renin release in both the filtering and nonfiltering kidney. Subsequent furosemide injection (5 mg/kg, iv) failed to increase renin release in the nonfiltering kidney. Similarly, after the infusion of lidocaine into the renal artery of the nonfiltering kidney (1 mg/kg per hour), furosemide did not alter renin release. In the denervated nonfiltering kidney, furosemide in a dose of 5 mg/kg, iv, increased renin release and decreased renal resistance. Treatment with dor rf,/-propranolol decreased renin release in five out of six denervated nonfiltering kidneys. Following propranolol, furosemide failed to increase renin release. These results demonstrate that the ability of </,/-propranolol to decrease renin release may be due partially to the membranestabilizing activity of the rf-isomer. Stimulation of renin release by furosemide occurs at both the vascular and macula densa sites which may act independently in the control of renin release. The data demonstrate that, whereas renal sympathetic innervation may modulate renin release under a variety of circumstances, this innervation is not an absolute requirement for renin release at the juxtaglomerular apparatus.

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