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高血压是心血管疾病的主要危险因素之一，降低血压对于减少心血管事件的发生有的重要的意义。高血压的病理生理机制复杂，其共同特点是活性氧的利用度增加，即氧化应激。在心血管系统中，活性氧在控制血管内皮功能、血管张力和心功能方面有着重要作用，并在炎症、肥大、增殖、凋亡、迁移、血管生成等病理生理过程中也发挥一定的作用，均参与了高血压所致的内皮功能障碍。虽然，动物实验研究的结果表明氧化应激是高血压的发病机制，但目前尚无明确的证据支持氧化应激在人群中导致高血压的发生。内皮功能障碍是血管内皮受到刺激后血管舒张反应下降，众多的研究证据表明其是介导高血压血管负面影响的重要机制之一，且有研究表明高血压相关的内皮功能障碍是由氧化应激所致。本文主要就高血压中的氧化应激、血管内皮功能障碍的实验研究、机制以及在高血压发生发展中两者的关系进行了综述。

英文摘要:

Hypertension is a major risk factor of cardiovascular disease, and the reduction of elevated blood pressure significantly reduced the risk of cardiovascular events. The pathophysiology of hypertension is complex and its the common process is increased bioavailability of reactive oxygen species (ROS), that is oxidative stress. In the cardiovascular system, ROS plays a physiological role in controlling endothelial function, vascular tone, and cardiac function, and a pathophysiological role in inflammation, hypertrophy, proliferation, migration, fibrosis, angiogenesis and so on, which also play roles in the endothelial dysfunction induced by hypertension. Although convincing data fromanimal studies support a causative role for oxidative stress in the pathogenesis of hypertension, there is no solid evidence that oxidative stress causes hypertension in humans yet. Endothelial dysfunction means reduced vasodilating response to endothelial stimuli. A large amount of evidences indicate that endothelial dysfunction is one of the mechanisms mediating the adverse vascular effects of hypertension. Hypertension-related endothelial dysfunction has been demonstrated to be the consequence of increased oxidative stress production in many studies．This review highlights the experimental studies and mechanism of oxidative stress and endothelial dysfunction in hypertension, and outlines the relationship between oxidative stress and endothelial dysfunction in the development of hypertension.

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