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-density lipoprotein (ox-LDL) in human saphenous veins and determined whether decreased availability of L-arginine was responsible for the impaired endothelial function. Human saphenous veins were obtained from white males undergoing coronary bypass surgery. We examined the effects of ox-LDL on ACh-induced endothelium-dependent relaxation, sodium nitroprusside-induced endothelium-independent relaxation and 5-HT-induced contraction. ACh-induced vasorelaxation in the presence of L-arginine and ox-LDL was also examined. In addition, we assessed the endothelial influence on the contractile response to 5-HT. ox-LDL significantly inhibited ACh-induced relaxation but did not affect sodium nitroprusside-induced relaxation. L-Arginine pretreatment did not prevent ox-LDL-induced impairment of the relaxation response to ACh. ox-LDL significantly potentiated 5-HT-induced contraction at concentrations between 3 x 10(-6) M and 10(-4) M, an effect that was endothelium-dependent. Denudation of endothelium also significantly enhanced the contractile response to 5-HT. These data suggest that ox-LDL impairs ACh-induced endothelium-dependent relaxation and enhances 5-HT-induced endothelium-dependent contraction in human saphenous vein. L-Arginine deficiency is not responsible for the endothelial dysfunction induced by ox-LDL in human saphenous vein.