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 NG-nitro-L-arginine (NOARG) on antidiuresis and norepinephrine (NE) overflow in anesthetized dogs, induced by renal nerve stimulation (RNS), with or without blockade of an action of endogenous angiotensin II (AII) on the AT1 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 differences in renal arteriovenous NE concentrations (NEC). Intrarenal arterial (i.r.a.) infusion of NOARG (40 micrograms/kg/min) significantly decreased RBF and UF, and increased FF, but did not alter GFR. When losartan 100 micrograms/kg/min was infused simultaneously, NOARG reduced RBF, UF, and GFR but had no effect on FF. With high-frequency RNS, NOARG enhanced the RNS-induced decreases in RBF, GFR, UF, and UNaV and the increases in NEC. During losartan infusion, NOARG-induced enhancements on renal actions in response to RNS were observed in a manner qualitatively similar to that without losartan. Most likely endogenous nitric oxide (NO) plays the role of inhibitory modulator of renal noradrenergic neurotransmission. Enhancement of renal noradrenergic neurotransmission induced by NO blockade is likely to be independent of an action of endogenous AII on the AT1 receptors.