INTERACTION BETWEEN NITRIC-OXIDE AND ANGIOTENSIN-II ON ANTIDIURESIS AND NOREPINEPHRINE OVERFLOW INDUCED BY STIMULATION OF RENAL NERVES IN ANESTHETIZED DOGS

We examined the effects of N-G-nitro-L-arginine (NOARG) on antidiuresi s and norepinephrine (NE) overflow in anesthetized dogs, induced by re nal nerve stimulation (RNS), with or without blockade of an action of endogenous angiotensin II (AII) on the AT, receptors by losartan. RNS (2.5-5.0 Hz) caused significant reductions in renal blood flow (RBF), glomerular filtration rate (GFR), filtration fraction (FF), urine flow (UF), and urinary excretion of sodium (UNaV) and increases in the dif ferences in renal arteriovenous NE concentrations (NEC). Intrarenal ar terial (i.r.a.) infusion of NOARG (40 mu g/kg/min) significantly decre ased RBF and UF, and increased FF, but did not alter GFR. When losarta n 100 mu g/kg/min was infused simultaneously, NOARG reduced RBF, UF, a nd GFR but had no effect on FF. With high-frequency RNS, NOARG enhance d the RNS-induced decreases in RBF, GFR, UF, and UNaV and the increase s in NEC. During losartan infusion, NOARG-induced enhancements on rena l actions in response to RNS were observed in a manner qualitatively s imilar to that without losartan. Most likely endogenous nitric oxide ( NO) plays the role of inhibitory modulator of renal noradrenergic neur otransmission. Enhancement of renal noradrenergic neurotransmission in duced by NO blockade is likely to be independent of an action of endog enous AII on the AT(1) receptors.