EFFECTS OF RENAL PERFUSION-PRESSURE ON RENAL INTERSTITIAL HYDROSTATIC-PRESSURE AND NA- ROLE OF ENDOTHELIUM-DERIVED NITRIC-OXIDE( EXCRETION )

The purpose of this study was to examine the role of endothelium-deriv ed 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-n itro-L-arginine methyl ester (L-NAME) at doses of 1, 5, and 50 mu g/kg /min, and in rats pretreated with L-NAME (5 mu g/kg/min) plus L-argini ne (10 mg/kg/min). The RPP was changed from 95 to 135 mm Hg by an elec tronically servo-controlled aortic occluder above the renal arteries i n all groups. Increasing RPP in control rats from 95 to 135 mm Hg incr eased RIHP (from 4.4 +/- 0.5 to 8.7 +/- 1.2 mm Hg), UNaV (from 2.37 +/ - 0.61 to 8.29 +/- 1.59 mu Eq/min), and fractional excretion of Li+ (f rom 38.0 +/- 2.5 to 51.4 +/- 6.0%). In rats pretreated with L-NAME (5 mu g/kg/min), increases in RPP from 95 to 135 mm Hg had no effect on R IHP (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 mu Eq/min). Although L-NAME did reduce r enal plasma flow and glomerular filtration rate, the autoregulatory re sponses 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 modul ating the effect of RPP on Na+ excretion by enhancing the transmission of RPP into the renal interstitium.