INTRARENAL NITRIC-OXIDE ACTIVITY AND PRESSURE NATRIURESIS IN ANESTHETIZED DOGS

Recent studies have indicated that changes in intrarenal nitric oxide (NO) production participate in mediating arterial pressure-induced cha nges in urinary sodium excretion. Until recently, however, the means t o measure changes in intrarenal NO activity in vivo have not been avai lable. For the present study, changes in renal tissue NO activities we re assessed directly using an NO-selective microelectrode inserted int o the cortical tissue of anesthetized dogs. Control studies demonstrat ed that the electrode was responsive to intrarenal bolus injections of acetylcholine and to the NO donor S-nitroso-acetylpenicillamine (SNAP ). Intrarenal nitro-L-arginine (50 mu g.kg(-1).min(-1)) decreased rena l tissue NO concentration by 593 +/- 127 nmol/L (P < 0.05; n=7). Infus ions of SNAP (1, 2, and 3 mu g.kg(-1).min(-1) for 25 minutes) in nitro -L-arginine-treated dogs (n=5) resulted in dose-dependent increases in renal tissue NO activity, which showed a positive correlation with ch anges in urinary excretion rates of NO metabolites, nitrates and nitri tes, (r=0.62, P < 0.05) and sodium (r=0.78, P < 0.01). During graded r eductions of renal arterial pressure within the autoregulatory range ( 144+/-3 to 73+/-2 mm Hg; n=10), there were decreases in tissue NO acti vity that were positively correlated with changes in renal arterial pr essure (r=0.45; P < 0.05), urinary nitrate/nitrite excretion (r=0.64, P < 0.005), and urinary sodium excretion (r=0.46; P < 0.05). These dat a support the hypothesis that acute changes in renal arterial pressure result in alterations in intrarenal NO activity, which may be respons ible for the associated changes in sodium excretion.