Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin
Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Am J Physiol Renal Physiol. 2015 Feb 1;308(3):F179-97. doi: 10.1152/ajprenal.00455.2014. Epub 2014 Oct 29.
The physiological evidence linking the production of superoxide, hydrogen peroxide, and nitric oxide in the renal medullary thick ascending limb of Henle (mTAL) to regulation of medullary blood flow, sodium homeostasis, and long-term control of blood pressure is summarized in this review. Data obtained largely from rats indicate that experimentally induced elevations of either superoxide or hydrogen peroxide in the renal medulla result in reduction of medullary blood flow, enhanced Na(+) reabsorption, and hypertension. A shift in the redox balance between nitric oxide and reactive oxygen species (ROS) is found to occur naturally in the Dahl salt-sensitive (SS) rat model, where selective reduction of ROS production in the renal medulla reduces salt-induced hypertension. Excess medullary production of ROS in SS rats emanates from the medullary thick ascending limbs of Henle [from both the mitochondria and membrane NAD(P)H oxidases] in response to increased delivery and reabsorption of excess sodium and water. There is evidence that ROS and perhaps other mediators such as ATP diffuse from the mTAL to surrounding vasa recta capillaries, resulting in medullary ischemia, which thereby contributes to hypertension.
本文综述了将超氧化物、过氧化氢和一氧化氮在亨利氏髓袢升支厚段（mTAL）中的产生与调节髓质血流、钠稳态和血压的长期控制联系起来的生理证据。这些数据主要来自大鼠，表明实验诱导的肾髓质中超氧化物或过氧化氢的升高导致髓质血流减少、钠重吸收增强和高血压。在 Dahl 盐敏感（SS）大鼠模型中，发现一氧化氮和活性氧（ROS）之间的氧化还原平衡自然发生变化，其中选择性减少肾髓质中 ROS 的产生可降低盐诱导的高血压。SS 大鼠肾髓质中超氧化物的过度产生源于亨利氏髓袢升支厚段[来自线粒体和膜 NAD(P)H 氧化酶]，这是对过量钠和水的输送和重吸收的反应。有证据表明，ROS 以及其他介质（如 ATP）可能从 mTAL 扩散到周围的直小血管，导致髓质缺血，从而导致高血压。
