Oxidative Stress and Hypertension: Current Concepts
Oxidative Stress and Hypertension: Current Concepts
复制标题
DOI：
10.1007/s11906-010-0100-z
复制
发表时间：
2010-04-01
影响因子：
5.6
通讯作者：
Touyz, Rhian M.
中科院分区：
文献类型：
--
作者：
Briones, Ana M.;Touyz, Rhian M.
高血压是导致肾功能衰竭、心血管疾病和中风的主要因素。这些病理改变与血管功能和结构改变有关，包括内皮功能障碍、收缩能力改变和血管重塑。这些现象的核心是氧化应激。激活促氧化酶的因素，如NADPH氧化酶，仍然不清楚，但可能涉及血管紧张素II、机械拉伸和炎性细胞因子。活性氧通过氧化还原依赖的信号通路调节细胞生长、收缩/扩张和炎症反应，从而影响血管、肾脏和心脏的功能和结构。来自分子和细胞实验的令人信服的数据，以及动物研究，暗示了氧化应激在高血压中的作用。然而，临床证据仍然存在争议。本文就氧化应激对血管的影响以及氧化损伤在实验性高血压和临床高血压中的意义进行了综述，并对氧化损伤的产生机制和氧化应激对血管的影响进行了综述。
Hypertension is a major contributor to the development of renal failure, cardiovascular disease, and stroke. These pathologies are associated with vascular functional and structural changes including endothelial dysfunction, altered contractility, and vascular remodeling. Central to these phenomena is oxidative stress. Factors that activate pro-oxidant enzymes, such as NADPH oxidase, remain poorly defined, but likely involve angiotensin II, mechanical stretch, and inflammatory cytokines. Reactive oxygen species influence vascular, renal, and cardiac function and structure by modulating cell growth, contraction/dilatation, and inflammatory responses via redox-dependent signaling pathways. Compelling data from molecular and cellular experiments, together with animal studies, implicate a role for oxidative stress in hypertension. However, the clinical evidence is still controversial. This review provides current insights on the mechanisms of the generation of reactive oxygen species and the vascular effects of oxidative stress and discusses the significance of oxidative damage in experimental and clinical hypertension.