Ellis Anthie, Triggle Chris R
Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, AB, Canada.
Can J Physiol Pharmacol. 2003 Nov;81(11):1013-28. doi: 10.1139/y03-106.
Opinions on the role of reactive oxygen species (ROS) in the vasculature have shifted in recent years, such that they are no longer merely regarded as indicators of cellular damage or byproducts of metabolism--they may also be putative mediators of physiological functions. Hydrogen peroxide (H2O2), in particular, can initiate vascular myocyte proliferation (and, incongruously, apoptosis), hyperplasia, cell adhesion, migration, and the regulation of smooth muscle tone. Endothelial cells express enzymes that produce ROS in response to various stimuli, and H2O2 is a potent relaxant of vascular smooth muscle. H2O2 itself can mediate endothelium-dependent relaxations in some vascular beds. Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. This review primarily focuses on the hypothesis that H2O2 is an EDHF in resistance arteries. Putative endothelial sources of H2O2 and the effects of H2O2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. Furthermore, given the perception that ROS can more likely elicit cytotoxic effects than perform signalling functions, the arguments for and against H2O2 being an endogenous vasodilator are assessed.
近年来，关于活性氧（ROS）在脉管系统中的作用的观点已经发生了转变，以至于它们不再仅仅被视为细胞损伤的指标或代谢副产物——它们也可能是生理功能的假定介质。特别是过氧化氢（H2O2），可以引发血管肌细胞增殖（并且，不协调的是，还有细胞凋亡）、增生、细胞黏附、迁移以及平滑肌张力的调节。内皮细胞表达能响应各种刺激产生ROS的酶，并且H2O2是血管平滑肌的一种强效舒张剂。H2O2自身可以介导某些血管床中的内皮依赖性舒张。尽管一氧化氮（NO）被公认为是一种内皮源性舒张因子，但同样确定的是，特别是在微脉管系统中，另一个因子，内皮源性超极化因子（EDHF），是血管舒张张力的一个重要决定因素。这篇综述主要关注H2O2是阻力动脉中的一种EDHF这一假说。讨论了H2O2可能的内皮来源以及H2O2对钾通道、钙稳态和血管平滑肌张力的影响。此外，鉴于人们认为ROS更可能引发细胞毒性作用而非执行信号传导功能，对支持和反对H2O2是一种内源性血管舒张剂的论据进行了评估。
