Ohashi Junko, Shimokawa Hiroaki
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine.
Nihon Rinsho. 2010 Apr;68(4):631-5.
Endothelium-derived hyperpolarizing factor (EDHF) plays an important role in modulating vascular tone. Although several candidates for EDHF have been proposed, we have demonstrated that endothelium-derived hydrogen peroxide(H2(0)2) is an EDHF in mouse and human mesenteric arteries and porcine coronary microvessels, which was subsequently confirmed by other investigators in human and canine coronary microvessels. We have also demonstrated that endothelial nitric oxide synthase (eNOS) is a major source of EDHF/H2(0)2, where Cu, Zn-SOD is involved. Furthermore, we showed that genetic disruption of all three NOS isoforms abolishes EDHF responses in mice and that endothelial NOSs system has diverse vasodilator functions depending on the vessel size, mainly contributing to EDHF/H2(0)2 responses in microvessels while serving as a NO-generating system in large arteries.
内皮衍生超极化因子（EDHF）在调节血管张力方面发挥着重要作用。尽管已经提出了几种EDHF的候选物质，但我们已经证明，内皮衍生的过氧化氢（H2O2）是小鼠和人肠系膜动脉以及猪冠状动脉微血管中的一种EDHF，随后其他研究者在人和犬的冠状动脉微血管中也证实了这一点。我们还证明，内皮型一氧化氮合酶（eNOS）是EDHF/H2O2的主要来源，其中铜锌超氧化物歧化酶（Cu，Zn-SOD）参与其中。此外，我们表明，所有三种一氧化氮合酶（NOS）亚型的基因敲除消除了小鼠的EDHF反应，并且内皮NOS系统根据血管大小具有不同的血管舒张功能，主要在微血管中促成EDHF/H2O2反应，而在大动脉中作为一氧化氮生成系统发挥作用。
