Role of nitric oxide in renal papillary blood flow and sodium excretion

Renal medullary interstitial infusion of N^G-nitro-L-arginine (120 μg/hr, n = 7) decreased papillary blood flow to 71±5% of control without altering outer cortical flow. Before N^G-nitro-L-arginine infusion, interstitial acetylcholine administration (200 μg/hr) increased cortical and papillary blood flow to 134±6% and 113±2% of control, respectively. After N^G-nitro-L-arginine administration, the vasodilator response to acetylcholine was abolished. In clearance experiments, renal medullary infusion of N^G-nitro-L-arginine (120 μg/hr, n = 7) significantly decreased total renal blood flow by 10%, renal interstitial fluid pressure by 23%, sodium excretion by 34%, and urine flow by 39% without altering glomerular filtration rate, fractional sodium and water excretion, blood pressure, or urine osmolality. These data indicate that selective inhibition of nitric oxide in the renal medullary vasculature reduces papillary blood flow, which is associated with decreased sodium and water excretion. We conclude that nitric oxide exerts a tonic influence on the renal medullary circulation.