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

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 ω -nitro- l -arginine methyl ester (50 μ g/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.