Reactive oxygen species (ROS) are produced by the aerobic metabolism. The imbalance between production of ROS and antioxidant defence in any cell compartment is associated with cell damage and may play an important role in the pathogenesis of renal disease. NADPH oxidase (NOX) family is the major ROS source in the vasculature and modulates renal perfusion. Upregulation of Ang II and adenosine activates NOX via AT1R and A1R in renal microvessels, leading to superoxide production. Oxidative stress in the kidney prompts renal vascular remodelling and increases preglomerular resistance. These are key elements in hypertension, acute and chronic kidney injury, as well as diabetic nephropathy. Renal afferent arterioles (Af), the primary resistance vessel in the kidney, fine tune renal hemodynamics and impact on blood pressure. Vice versa, ROS increase hypertension and diabetes, resulting in upregulation of Af vasoconstriction, enhancement of myogenic responses and change of tubuloglomerular feedback (TGF), which further promotes hypertension and diabetic nephropathy. In the following, we highlight oxidative stress in the function and dysfunction of renal hemodynamics. The renal microcirculatory alterations brought about by ROS importantly contribute to the pathophysiology of kidney injury, hypertension and diabetes.

中文翻译：

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活性氧在肾脏血管功能中的作用。

有氧代谢产生活性氧（ROS）。ROS的产生与任何细胞区室中的抗氧化剂防御之间的不平衡与细胞损伤有关，并且可能在肾脏疾病的发病机理中起重要作用。NADPH氧化酶（NOX）家族是脉管系统中主要的ROS来源，可调节肾脏灌注。Ang II和腺苷的上调通过肾微血管中的AT1R和A1R激活NOX，从而导致超氧化物的产生。肾脏中的氧化应激会促使肾脏血管重塑并增加肾小球前阻力。这些是高血压，急性和慢性肾脏损伤以及糖尿病性肾病的关键因素。肾传入小动脉（Af）是肾脏中的主要阻力血管，可微调肾脏血液动力学和对血压的影响。反之亦然，ROS增加高血压和糖尿病，导致Af血管收缩的上调，肌原性反应的增强和肾小管肾小球反馈（TGF）的改变，这进一步促进了高血压和糖尿病性肾病。在下文中，我们重点介绍了氧化应激在肾血液动力学功能和功能障碍中的作用。ROS引起的肾脏微循环改变对肾脏损伤，高血压和糖尿病的病理生理起重要作用。