Hypercholesterolemia suppresses inwardly rectifying K+ channels in aortic endothelium in vitro and in vivo

摘要: Inwardly rectifying K+ (Kir) channels are responsible for maintaining endothelial membrane potential and play a key role in endothelium-dependent vasorelaxation. In this study, we show that Kir suppressed by hypercholesterolemic levels of lipoproteins vitro serum hypercholesterolemia vivo. Specifically, exposing human aortic cells to acetylated low-density lipoprotein or very low density resulted time- concentration-dependent decrease current correlated with the degree cholesterol loading. The suppression was fully reversible depletion. Furthermore, depolarization potential. Most important, flow sensitivity currents also impaired flow-induced increase 70%, hyperpolarization almost completely abrogated. vivo strongly suppresses causes shift potential, as determined comparing freshly isolated from healthy pigs. Therefore, suggest is one important factors hypercholesterolemia-induced dysfunction.