Shimokawa Hiroaki, Matoba Tetsuya
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidaishi, Higashi-ku, Fukuoka 812-8582, Japan.
Pharmacol Res. 2004 Jun;49(6):543-9. doi: 10.1016/j.phrs.2003.10.016.
Vascular endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several vasodilating factors, such as prostacyclin, nitric oxide (NO), and a yet unidentified endothelium-derived hyperpolarizing factor (EDHF). Possible candidates for EDHF include epoxyeicosatrienoic acids (EETs), endothelium-derived potassium ions (K(+)), and as we have recently identified, hydrogen peroxide (H2O2). Electrical communication between endothelial and smooth muscle cells through gap junctions has also been suggested to be involved in endothelium-dependent hyperpolarization. Among the above candidates, the H2O2 hypothesis well explains the pathophysiological interactions between NO and EDHF and re-highlights the physiological roles of the reactive oxygen species (ROS) in endothelium-dependent vascular responses. This brief review summarizes our current knowledge about H2O2 as an EDHF, with special reference to its production by the endothelium, its action on membrane potentials and its pathophysiological roles.
血管内皮通过合成和释放几种血管舒张因子，如前列环素、一氧化氮（NO）和一种尚未明确的内皮衍生超极化因子（EDHF），在维持血管稳态中发挥重要作用。EDHF的可能候选物包括环氧二十碳三烯酸（EETs）、内皮衍生的钾离子（K(+)），以及正如我们最近所发现的过氧化氢（H2O2）。内皮细胞与平滑肌细胞之间通过缝隙连接的电通讯也被认为参与了内皮依赖性超极化。在上述候选物中，H2O2假说很好地解释了NO与EDHF之间的病理生理相互作用，并再次突出了活性氧（ROS）在内皮依赖性血管反应中的生理作用。这篇简短的综述总结了我们目前关于H2O2作为EDHF的知识，特别提及了它由内皮产生的过程、对膜电位的作用及其病理生理作用。
