RENAL EFFECTS OF THE NITRIC-OXIDE SYNTHASE INHIBITOR, L-NG-NITROARGINE, IN DOGS

L-N(G)-Nitroarginine (LNNA), an analog of L-arginine, was infused into the renal artery of anesthetized dogs to assess the contribution of nitric oxide production in the regulation of renal hemodynamics and urine formation. Following intrarenal arterial infusion of LNNA (15-mu-g/kg/min) for 25 min, renal blood flow (RBF) gradually decreased and there was no reversion even 60 min after cessation of infusion, with no change in mean arterial blood pressure (MBP) and heart rate. Urine flow (UF) decreased while the glomerular filtration rate (GFR) did not change. The highest dose of LNNA (75-mu-g/kg/min) remarkably decreased RBF and increased MBP. The renal vasoconstriction and pressor responses induced by the highest dose of LNNA were significantly antagonized by an intravenous administration Of L-arginine (100 mg/kg/min). LNNA is characterized as a potent and long-lasting renal vasoconstrictor and decreases GFR, UF, and sodium excretion. It is suggested that nitric oxide produced in the kidney may have a significant role in the regulation of basal renal circulation and exert diuresis and natriuresis.