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原发性高血压中活性氧与多巴胺受体功能

Reactive oxygen species and dopamine receptor function in essential hypertension.

作者信息

Zeng Chunyu, Villar Van Anthony M, Yu Peiying, Zhou Lin, Jose Pedro A

机构信息

Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, PR China.

出版信息

Clin Exp Hypertens. 2009 Apr;31(2):156-78. doi: 10.1080/10641960802621283.

Abstract

Essential hypertension is a major risk factor for stroke, myocardial infarction, and heart and kidney failure. Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones and humoral factors. However, the mechanisms leading to impaired dopamine receptor function in hypertension states are not clear. Compelling experimental evidence indicates a role of reactive oxygen species (ROS) in hypertension, and there are increasing pieces of evidence showing that in conditions associated with oxidative stress, which is present in hypertensive states, dopamine receptor effects, such as natriuresis, diuresis, and vasodilation, are impaired. The goal of this review is to present experimental evidence that has led to the conclusion that decreased dopamine receptor function increases ROS activity and vice versa. Decreased dopamine receptor function and increased ROS production, working in concert or independent of each other, contribute to the pathogenesis of essential hypertension.

摘要

原发性高血压是中风、心肌梗死以及心脏和肾衰竭的主要危险因素。多巴胺通过调节上皮钠转运以及与血管活性激素和体液因子相互作用,在高血压发病机制中发挥重要作用。然而,高血压状态下导致多巴胺受体功能受损的机制尚不清楚。有力的实验证据表明活性氧(ROS)在高血压中起作用,并且越来越多的证据表明,在高血压状态下存在的与氧化应激相关的情况下,多巴胺受体的作用,如利钠、利尿和血管舒张,会受到损害。本综述的目的是展示实验证据,这些证据得出了多巴胺受体功能降低会增加ROS活性,反之亦然的结论。多巴胺受体功能降低和ROS产生增加,彼此协同或独立作用,共同促成原发性高血压的发病机制。

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