Nitric Oxide Dependency of Arterial Pressure–Induced Changes in Renal Interstitial Hydrostatic Pressure in Dogs

Abstract

Abstract —A direct relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure (RIHP) has been shown under conditions of efficient renal blood flow autoregulation. Experiments were performed in six anesthetized dogs to evaluate whether these RIHP responses to changes in RAP were modified during nitric oxide (NO) inhibition with nitro- l -arginine (NLA) or after administration of NO donor agents. A microtip catheter transducer was placed underneath the renal capsule to measure RIHP. Stepwise reductions in RAP (140 to 80 mm Hg) during control conditions resulted in decreases in RIHP from its basal value of 4.7±1.1 mm Hg with a slope of 0.04±0.026 mm Hg · mm Hg − 1 along with decreases in urinary nitrate/nitrite excretion rate (U NOx V). Renal cortical and medullary blood flows, measured by laser-Doppler flowmetry, exhibited high autoregulatory efficiency over this RAP range. The changes in RIHP during alterations in RAP were positively correlated ( r =0.743; P <0.001) with the changes in U NOx V but not with cortical or medullary blood flow. NLA infusion decreased RIHP to 1.9±0.5 mm Hg and also reduced U NOx V from 1.8±0.2 to 0.9±0.01 nmol · min − 1 · g − 1 . Infusion of NO donors restored RIHP (4.3±0.9 mm Hg) and U NOx V (1.5±0.2 nmol · min − 1 · g − 1 ). During NLA infusion, the RIHP responses to reductions in RAP were markedly attenuated and were not restored even during constant-rate infusion of NO donors. The results suggest that changes in RIHP in response to alterations in RAP are associated with changes in intrarenal NO, suggesting a direct effect of NO to regulate RIHP.