Department of Clinical Nutrition, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Division of Renal Diseases & Hypertension, Department of Medicine, The George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.
Antioxid Redox Signal. 2021 Mar 20;34(9):716-735. doi: 10.1089/ars.2020.8106. Epub 2020 May 29.
The kidney plays an important role in the long-term control of blood pressure. Oxidative stress is one of the fundamental mechanisms responsible for the development of hypertension. Dopamine, five subtypes of receptors, plays an important role in the control of blood pressure by various mechanisms, including the inhibition of oxidative stress. Dopamine receptors exert their regulatory function to decrease the oxidative stress in the kidney and ultimately maintain normal sodium balance and blood pressure homeostasis. An aberration of this regulation may be involved in the pathogenesis of hypertension. Our present article reviews the important role of oxidative stress and intrarenal dopaminergic system in the regulation of blood pressure, summarizes the current knowledge on renal dopamine receptor-mediated antioxidation, including decreasing reactive oxygen species production, inhibiting pro-oxidant enzyme nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, and stimulating antioxidative enzymes, and also discusses its underlying mechanisms, including the increased activity of G protein-coupled receptor kinase 4 (GRK4) and abnormal trafficking of renal dopamine receptors in hypertensive status. Identifying the mechanisms of renal dopamine receptors in the regulation of oxidative stress and their contribution to the pathogenesis of hypertension remains an important research focus. Increased understanding of the role of reciprocal regulation between renal dopamine receptors and oxidative stress in the regulation of blood pressure may give us novel insights into the pathogenesis of hypertension and provide a new treatment strategy for hypertension.
肾脏在长期血压控制中发挥着重要作用。氧化应激是导致高血压发生的基本机制之一。多巴胺通过多种机制（包括抑制氧化应激）在血压控制中发挥重要作用，其有 5 种不同的受体亚型。多巴胺受体通过调节作用减少肾脏中的氧化应激，最终维持正常的钠平衡和血压稳态。这种调节的失常可能与高血压的发病机制有关。
我们目前的文章综述了氧化应激和肾内多巴胺能系统在血压调节中的重要作用，总结了目前关于肾多巴胺受体介导的抗氧化作用的知识，包括减少活性氧的产生、抑制促氧化剂烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶以及刺激抗氧化酶，并讨论了其潜在机制，包括 G 蛋白偶联受体激酶 4（GRK4）活性增加和高血压状态下肾多巴胺受体的异常转运。
确定肾多巴胺受体在氧化应激调节中的作用机制及其在高血压发病机制中的作用仍然是一个重要的研究重点。增加对肾多巴胺受体与氧化应激之间相互调节在血压调节中的作用的理解，可能为我们深入了解高血压的发病机制提供新的见解，并为高血压的治疗提供新的策略。
