Protecting endothelial function: A novel therapeutic target of ATP-sensitive potassium channel openers

Abstract

See article by Wang et al. [7] (pages 497–503) in this issue . Endothelial dysfunction is commonly observed in patients with hypertension, type II diabetes mellitus, and hypercholesteremia and is considered to be an early event in the changes accompanying atherosclerosis [1,2]. Disruption of normal endothelial function leads to loss of vasomotor control, reduced production of nitric oxide (NO), formation of a procoagulant surface, and promotion of inflammation [1,2]. These events may lead to destabilization of atherosclerotic plaques and could cause acute coronary syndrome. Indeed, recent clinical studies have demonstrated that endothelial dysfunction is a predictor for the development of cardiovascular events [3,4]. Endothelial cells express a diverse array of ion channels which play important roles in modulating cell function [5]. Since Noma first identified ATP-sensitive potassium (KATP) channels in cardiac myocytes, the physiological roles of KATP channels have been extensively studied in cardiac muscle and other tissues [5,6]. Endothelial KATP channels contribute to maintaining the resting membrane potential. In addition, they also regulate intracellular Ca2+ levels that affect the production and release of endothelial autacoids, … *Corresponding author. Tel.: +81 6 6879 3635; fax: +81 6 6879 3634. Email address: mhori{at}medone.med.osaka-u.ac.jp