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 rain) 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 μg/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.