EFFECT OF SODIUM-NITROPRUSSIDE ON NOREPINEPHRINE OVERFLOW AND ANTIDIURESIS INDUCED BY STIMULATION OF RENAL NERVES IN ANESTHETIZED DOGS

To investigate the role of nitric oxide (NO) in the regulation of rena l sympathetic nerve activity and renal function, we examined the effec t of sodium nitroprusside (SNP), a NO donor, on renal actions induced by renal nerve stimulation (RNS) in anesthetized dogs, with or without blockade of an endogenous NO generation by N-G-nitro-L-arginine (NOAR G), a NO synthase inhibitor. Low-frequency RNS (0.5-2.0 Hz) enhanced t he rate of norepinephrine secretion rate (NESR) from the kidney and de creased urine flow (UF), urinary excretion of sodium (UNaV), and fract ional excretion of sodium (FE(Na)), without affecting systemic and ren al hemodynamics. The intrarenal arterial infusion of SNP, in a dose (1 mu g/kg/min) that does not affect renal hemodynamics and urine format ion at the basal level, significantly attenuated the RNS-induced decre ases in UF, UNaV and FE(Na). The intrarenal administration of NOARG (4 0 mu g/kg/min) elicited renal vasoconstriction and reduced urine forma tion. RNS during NOARG administration reduced renal blood flow (RBF) a nd glomerular filtration rate (GFR) and augmented RNS-induced reductio n in urine formation. Simultaneously, NESR was markedly enhanced. The renal actions observed with NOARG administration during control and RN S periods were almost completely abolished by treatment with SNP. Ther efore, we suggest that NO plays an important role in the regulation of renal function. Endogenous NO probably functions as an inhibitory mod ulator of renal noradrenergic neurotransmission at the prejunctional l evel.