INFLUENCE OF ENDOTHELIUM-DERIVED RELAXING FACTOR ON RENAL MICROVESSELS AND PRESSURE-DEPENDENT VASODILATION

The influence of endothelium-derived relaxing factor (EDRF) on renal m icrovessels and autoregulation was visualized in vivo, in the split hy dronephrotic kidney of rats. EDRF synthesis was inhibited by local adm inistration of 10(-5) M N(G)-nitro-L-arginine methyl ester (L-NAME). D iameters of arcuate arteries decreased by 17%. In cortical vessels eff erent arterioles constricted more (13-16%) than interlobular arteries and afferent arterioles (7-12%). Cortical glomerular blood flow (GBF) decreased by 46% after L-NAME. A similar behavior of blood flow and va scular diameters was also observed in juxtamedullary (JM) arterioles. The responses to acetylcholine but not to sodium nitroprusside were at tenuated after L-NAME. After local administration of L-arginine (10(-3 ) M) diameters of all vessels and GBF increased, vascular responses to L-NAME were blunted. Step-wise reduction of renal perfusion pressure revealed that autoregulation was preserved in cortical vessels after L -NAME. In JM arterioles, which do not autoregulate in female Wistar ra ts, autoregulation of GBF was enhanced after L-NAME. These data sugges t that tonic formation of EDRF influences basal renal hemodynamics to a considerable extent. EDRF may also impair autoregulation of JM glome ruli without disturbing autoregulation of cortical glomeruli.