A nitric oxide donor NOC 7 suppresses renal responses induced by norepinephrine and angiotensin II in the NO-depleted denevated rabbit kidney

European Journal of Pharmacology
N OnoS Satoh

Abstract

Intrarenal arterial infusion of norepinephrine (30 ng/kg per min) or of angiotensin II (4 ng/kg per min) reduced the glomerular filtration rate and urinary Na+ excretion in denervated kidneys of anesthetized rabbits pretreated intrarenally with a nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine methyl ester (50 microg/kg per min). Angiotensin II but not norepinephrine reduced fractional Na+ excretion. Intrarenal administration of a spontaneous NO donor 1-hydroxy-2-oxo-3-(N-methyl-3-aminopropyl)-3-methyl-1-triazene (NOC 7, 30 ng/kg per min) in L-NAME pretreated kidneys did not affect basal values, but attenuated the reduction in urinary Na+ excretion induced by these agonists without affecting the angiotensin II-induced reduction in glomerular filtration rate. The results suggest that NOC 7 can suppress the norepinephrine-induced hypofiltration and the angiotensin II-evoked tubular reabsorption and thereby attenuates the agonist-induced antinatriuresis in the denervated and endogenous NO-depleted rabbit kidney.

References

Dec 1, 1990·Journal of the American Society of Nephrology : JASN·C BaylisK Engels
Apr 18, 1997·European Journal of Pharmacology·Y AdachiS Satoh

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Citations

Dec 1, 1998·European Journal of Pharmacology·N OnoS Satoh
Mar 3, 2007·Pharmacological Reviews·Noboru TodaTomio Okamura
Apr 18, 2002·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Hideki TaniokaSusumu Satoh

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