RT Journal Article
SR Electronic
T1 Oxidized Low-Density Lipoprotein Inhibits Acetylcholine-Induced Vasorelaxation and Increases 5-HT-Induced Vasoconstriction in Isolated Human Saphenous Vein
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 637
OP 643
VO 284
IS 2
A1 Zhao, Lifan
A1 Tackett, Randall L.
YR 1998
UL http://jpet.aspetjournals.org/content/284/2/637.abstract
AB 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 × 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. The American Society for Pharmacology and Experimental Therapeutics