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首页> 外文期刊>American Journal of Physiology >NADPH oxidase contributes to renal damage and dysfunction in Dahl salt-sensitive hypertension
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NADPH oxidase contributes to renal damage and dysfunction in Dahl salt-sensitive hypertension

机译：NADPH氧化酶有助于达尔盐敏感性高血压的肾脏损害和功能障碍

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NADPH oxidase contributes to renal damage and dysfunction in Dahl salt-sensitive hypertension. Am J Physiol Regul Integr Comp Physiol 295: R1858-R1865, 2008. First published October 15, 2008; doi:10.1152/ajpregu.90650.2008.-The goal of this study was to test the hypothesis that NADPH oxidase contributes importantly to renal cortical oxidative stress and inflammation, as well as renal damage and dysfunction, and increases in arterial pressure. Fifty-four 7- to 8-wk-old Dahl salt-sensitive (S) or R/Rapp strain rats were maintained for 5 wk on a high sodium (8%) or high sodium + apocynin (1.5 mmol/1 in drinking water). Arterial and venous catheters were implanted on day 21. By day 35 in the high-Na S rats, mRNA expression of renal cortical gp91phox, p22phox, p47phox, and p67phox NADPH subunits in S rats increased markedly, and treatment of high-Na S rats with the NADPH oxidase inhibitor apocynin resulted in significant decreases in mRNA expression of these NADPH oxidase subunits. At the same time, in apocy-nin-treated S rats 1) renal cortical GSH/GSSG ratio increased, 2) renal cortical Oz'~ release and NADPH oxidase activity decreased, and 3) renal glomerular and interstitial damage markedly fell. Apocynin also decreased renal cortical monocyte/macrophage infiltration, and apocynin, but not the xanthine oxidase inhibitor allopurinol, attenuated decreases in renal hemodynamics and lowered arterial pressure. These data suggest that NADPH oxidase plays an important role in causing renal cortical oxidative stress and inflammation, which lead to decreases in renal hemodynamics, renal cortical damage, and increases in arterial pressure#
机译：NADPH氧化酶在Dahl盐敏感性高血压中导致肾脏损害和功能障碍。 Am J Physiol Regul Integr Comp Physiol 295：R1858-R1865，2008年。2008年10月15日首次发布。 doi：10.1152 / ajpregu.90650.2008.-本研究的目的是检验以下假设：NADPH氧化酶对肾皮质氧化应激和炎症，肾损害和功能异常以及动脉压升高起重要作用。在高钠（8％）或高钠+阿朴西宁（1.5 mmol / 1在饮用水中）维持54只7至8周大的Dahl盐敏感性（S）或R / Rapp品系大鼠5周）。在第21天植入动脉和静脉导管。到高Na S大鼠，到第35天，S大鼠中肾皮质gp91phox，p22phox，p47phox和p67phox NADPH亚基的mRNA表达显着增加，并且治疗高Na S大鼠NADPH氧化酶抑制剂Apocynin导致这些NADPH氧化酶亚基的mRNA表达显着下降。同时，经载脂蛋白处理的S大鼠1）肾皮质GSH / GSSG比增加，2）肾皮质Oz'释放和NADPH氧化酶活性降低，以及3）肾小球和间质损伤明显降低。阿波西宁还减少了肾皮质单核细胞/巨噬细胞的浸润，而阿朴西宁（但不是黄嘌呤氧化酶抑制剂别嘌呤醇）减少了肾血流动力学的下降并降低了动脉压。这些数据表明，NADPH氧化酶在引起肾皮质氧化应激和炎症中起重要作用，从而导致肾血流动力学下降，肾皮质损害和动脉压升高＃

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