THE EFFECTS OF N-G-NITRO-L-ARGININE, A NITRIC-OXIDE SYNTHASE INHIBITOR, ON NOREPINEPHRINE OVERFLOW AND ANTIDIURESIS INDUCED BY STIMULATION OF RENAL NERVES IN ANESTHETIZED DOGS

We examined the involvement of endogenous nitric oxide (NO) in noradre nergic neurotransmission and renal function in anesthetized dogs, by u sing N-G-nitro-L-arginine (NOARG), a NO synthase inhibitor. Renal nerv e stimulation (RNS) produced the frequency-dependent increase in the r ate of norepinephrine secretion. The low frequency RNS (0.5-2.0 Hz) de creased urine flow and urinary excretion of sodium, without affecting renal hemodynamics. High frequency RNS (2.5-5.0 Hz) caused a more pote nt antidiuresis and renal vasoconstriction that resulted in reductions in renal blood flow and glomerular filtration rate. Intrarenal arteri al infusion of NOARG, at a dose (10 mu g/kg/min) which had no effect o n renal hemodynamics, significantly enhanced the RNS-induced reduction s of urine formation and renal vasoconstriction and increments in nore pinephrine secretion rate. Qualitatively similar results were observed with a higher dose of NOARG (40 mu g/kg/min), although this dose did decrease basal levels of renal blood flow and urine flow. Enhancement of NOARG on RNS-induced actions was abolished by the simultaneous admi nistration of L-arginine. Endogenous NO probably has a role as inhibit ory modulator of renal noradrenergic neurotransmission.