The Japanese Journal of Nephrology
Online ISSN : 1884-0728
Print ISSN : 0385-2385
ISSN-L : 0385-2385
Effect of Isoproterenol on Renin Release
Takashi Inoue
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1973 Volume 15 Issue 8 Pages 745-762

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Abstract

Effects of intrarenol isoproterenol (IP) infusion (0.1, 0.05 and 0.01μg/kg/min) on renal functions and renin secretion were studied in the anesthetized dog. Intrarenal infusion of IP at doses of 0.1 and 0.05 μg/kg/min caused a slight decrease in systemic blood pressure (BP) but an increase in renal blood flow (RBF) accompanying by increase in urine flow (UF) and sodium excretion. At dose of 0.01 μg/kg/min, change in BP was not recognized but RBF and glomerular filtration rate (GFR) significantly increased concomitant with increases of OF and sodium excretion. The all three doses of IP produced increases in both systemic arterial and renal venous plasma renin activity (PRA) resulting in a significant increase of the renal venous-arterial difference of PRA. Thus renin secretion rate (RSR), the product of renal plasma flow and renal venous-arterial difference of PRA, significantly increased. The intrarenal distribution of blood flow during IP infusion (0.01 μg/kg/min) was determined by means of radioactive microsphere method. IP caused significant increase in RBF and RSR but no change in the intrarenal distribution of blood flow. Following intrarenal arterial injection of propranolol (1 mg), IP (0.01 μg/kg/min) caused no change in RBF and GFR, but produced a slight and significant increase of sodium excretion. While, intrarenal infusion of propranolol (1 μg/kg/min) completely blocked increase in RBF, GER, OF and sodium excretion induced by IP. Those propranolol administrations supressed both systemic arterial and renal venous PRA, and the latter was significantly lowered resulting in significant decrease in RSR. Furthermore, both PRA and RSR were not altered by IP in the presence of propranolol. Diuretic and natriuretic effects of IP seems to be due to increase in GFR and direct tubular effect was also suggested. An increase of RSR responded to IP was likely independent from the change in renal hemodynamics and tubular function. Thus it is suggested that IP stimulates renin release via β-adrenergic receptor in the kidney.

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