Effects of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Na ⁺ Excretion: Role of Endothelium-Derived Nitric Oxide

Abstract

The purpose of this study was to examine the role of endothelium-derived nitric oxide in modulating the effect of renal perfusion pressure (RPP) on renal interstitial hydrostatic pressure (RIHP) and urinary Na⁺ excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and Na⁺ and Li⁺ excretions were determined in control Sprague-Dawley rats, in Sprague-Dawley rats pretreated with intravenous infusion of N^G-nitro- L-arginine methyl ester ( L-NAME) at doses of 1, 5, and 50 µg/kg/min, and in rats pretreated with L-NAME (5 µg/kg/min) plus L-arginine (10 mg/kg/min). The RPP was changed from 95 to 135 mm Hg by an electronically servo-controlled aortic occluder above the renal arteries in all groups. Increasing RPP in control rats from 95 to 135 mm Hg increased RIHP (from 4.4 ± 0.5 to 8.7 ± 1.2 mm Hg), UNaV (from 2.37 ± 0.61 to 8.29 ± 1.59 µEq/min), and fractional excretion of Li⁺ (from 38.0 ± 2.5 to 51.4 ± 6.0%). In rats pretreated with L-NAME (5 µg/kg/min), increases in RPP from 95 to 135 mm Hg had no effect on RIHP (from 1.6 ± 0.4 to 2.2 ± 0.6 mm Hg) or fractional excretion of Li⁺ and markedly attenuated pressure-natriuresis relationship (from 1.84 ± 0.50 to 2.88 ± 0.65 µEq/min). Although L-NAME did reduce renal plasma flow and glomerular filtration rate, the autoregulatory responses to RPP were maintained. In rats pretreated with L-NAME plus L-arginine, RIHP, UNaV, and fractional excretion of Li⁺ responses to RPP were similar to the control rats. The results of this study indicate that endothelium-derived nitric oxide plays an important role in modulating the effect of RPP on Na⁺ excretion by enhancing the transmission of RPP into the renal interstitium.