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
Y. Egi et al., 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, The Journal of pharmacology and experimental therapeutics, 269(2), 1994, pp. 529-535
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.