OXIDIZED LOW-DENSITY-LIPOPROTEIN INHIBITS ACETYLCHOLINE-INDUCED VASORELAXATION AND INCREASES 5-HT-INDUCED VASOCONSTRICTION IN ISOLATED HUMAN SAPHENOUS-VEIN

The present study determined the vasomotor effects of oxidized low-den sity lipoprotein (ox-LDL) in human saphenous veins and determined whet her decreased availability of L-arginine was responsible for the impai red endothelial function. Human saphenous veins were obtained from whi te males undergoing coronary bypass surgery. We examined the effects o f ox-LDL on ACh-induced endothelium-dependent relaxation, sodium nitro prusside-induced endothelium-independent relaxation and 5-HT-induced c ontraction. ACh-induced vasorelaxation in the presence of L-arginine a nd ox-LDL was also examined. In addition, we assessed the endothelial influence or, the contractile response to 5-HT. ox-LDL significantly i nhibited ACh-induced relaxation but did not affect sodium nitroprussid e-induced relaxation. L-Arginine pretreatment did not prevent ox-LDL-i nduced impairment of the relaxation response to ACh. ox-LDL significan tly potentiated 5-HT-induced contraction at concentrations between 3 x 10(-6) M and 10(-4) M, an effect that was endothelium-dependent. Denu dation of endothelium also significantly/enhanced the contractile resp onse to 5-HT. These data suggest that ox-LDL impairs ACh-induced endot helium-dependent relaxation and enhances 5-HT-induced endothelium-depe ndent contraction in human saphenous vein. L-Arginine deficiency is no t responsible for the endothelial dysfunction induced by ox-LDL in hum an saphenous vein.