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 renal sympathetic nerve activity and renal function, we examined the effect 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 NG-nitro-L-arginine (NOARG), a NO synthase inhibitor. Low-frequency RNS (0.5-2.0 Hz) enhanced the rate of norepinephrine secretion rate (NESR) from the kidney and decreased urine flow (UF), urinary excretion of sodium (U(Na)V), and fractional excretion of sodium (FENa, without affecting systemic and renal hemodynamics. The intrarenal arterial infusion of SNP, in a dose (1 mu g/kg/min) that does not affect renal hemodynamics and urine formation at the basal level, significantly attenuated the RNS-induced decreases in UF, UNa V and FENa. The intrarenal administration of NOARG (40 mu g/kg/min) elicited renal vasoconstriction and reduced urine formation. RNS during NOARG administration reduced renal blood flow (RBF) and glomerular filtration rate (GFR) and augmented RNS-induced reduction in urine formation. Simultaneously, NESR was markedly enhanced. The renal actions observed with NOARG administration during control and RNS periods were almost completely abolished by treatment with SNP. Therefore, we suggest that NO plays an important role in the regulation of renal function. Endogenous NO probably functions as an inhibitory modulator of renal noradrenergic neurotransmission at the prejunctional level.