Higashi Yukihito, Yoshizumi Masao
Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical Sciences, Hiroshima University.
Nihon Rinsho. 2004 Jan;62(1):49-55.
Hypertension is a risk factor for cardiovascular and cerebrovascular outcome. Hypertension is associated with oxidative stress. Alteration in endothelial function is an initial step in the pathogenesis of atherosclerosis. A balance between ambient levels of super oxide and released nitric oxide(NO) plays an important role in the maintenance of endothelial function. It is well known that reactive oxygen species, including hydroxy radicals, directly scavenge NO and produce toxic peroxynitrite. Angiotensin II and mechanical stress generate the reactive oxygen species through the activation of NADH/NADPH oxidase in hypertension. Several investigators have shown that oxidative stress is involved in enhanced vascular growth, vascular inflammation, and impaired endothelium-dependent in hypertension. In this review, we would like to explain the role of oxidative stress in hypertensive organ damages.
高血压是心血管和脑血管疾病的危险因素。高血压与氧化应激有关。内皮功能改变是动脉粥样硬化发病机制的起始步骤。超氧化物的环境水平与释放的一氧化氮（NO）之间的平衡在维持内皮功能中起重要作用。众所周知，包括羟基自由基在内的活性氧会直接清除NO并产生有毒的过氧亚硝酸盐。在高血压中，血管紧张素II和机械应激通过激活NADH/NADPH氧化酶产生活性氧。几位研究者表明，氧化应激参与了高血压中血管生长增强、血管炎症以及内皮依赖性受损的过程。在本综述中，我们将解释氧化应激在高血压性器官损伤中的作用。
