Control of renin release. Effects of d-propranolol and renal denervation on furosemide-induced renin release in the dog.

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Abstract
The effects of d-propranolol and renal denervation were examined on furosemide-induced renin release in the anesthetized dog. d-Propranolol possess only membrane-stabilizing properties, whereas the l-isomer produces .beta.-adrenergic blockade. To separate the vascular and macula dense mechanisms of the juxtaglomerular apparatus effectively nonfiltering kidneys were produced by combining 2.5 h 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 h ischemic interval. Administration of d-propranolol in a priming dose of 1 mg/kg, i.v., followed by an i.v. infusion of 1 mg/kg per h decreased renin release in the filtering and nonfiltering kidney. Subsequent furosemide injection (5 mg/kg i.v.) failed to increase renin release in the nonfiltering kidney. After the infusion of lidocaine into the renal artery of the nonfiltering kidney (1 mg/kg per h), furosemide did not alter renin release. In the denervated nonfiltering kidney, furosemide in a dose of 5 mg/kg, i.v., increased renin release and decreased renal resistance. Treatment with d- or d,l-propranolol decreased renin release in 5 out of 6 denervated nonfiltering kidneys. Following propranolol, furosemide failed to increase renin release. The ability of d,l-propranolol to decrease renin release may be due partially to the membrane-stabilizing activity of the d-isomer. Stimulation of renin release by furosemide occurs at the vascular and macula densa sites which may act independently in control of renin release. Whereas renal sympathetic innervation may modulate renin release under a variety of circumstances, this innervation apparently is not an absolute requirement for renin release at the juxtaglomerular apparatus.