过氧亚硝酸盐
伊诺斯
一氧化氮
一氧化氮合酶
超氧化物
血管舒张
氧化应激
精氨酸酶
内皮功能障碍
内科学
内皮
一氧化氮合酶Ⅲ型
内皮一氧化氮合酶
化学
药理学
内分泌学
医学
酶
生物化学
精氨酸
氨基酸
作者
Gustavo H. Oliveira-Paula,Riccardo Lacchini,José Eduardo Tanus‐Santos
出处
期刊:Current Drug Targets
[Bentham Science]
日期:2014-01-31
卷期号:15 (2): 164-174
被引量:62
标识
DOI:10.2174/13894501113146660227
摘要
Nitric oxide (NO) is an important vasodilator produced by vascular endothelium. Its enzymatic formation is derived from three different synthases: neuronal (nNOS), endothelial (eNOS) and inducible (iNOS) synthases. While relatively small amounts of NO produced by eNOS are important to cardiovascular homeostasis, high NO levels produced associated with iNOS activity may have detrimental consequences to the cardiovascular system and contribute to hypertension. In this article, we reviewed current literature and found mounting evidence indicating that increased iNOS expression and activity contribute to the pathogenesis of hypertension and its complications. Excessive amounts of NO produced by iNOS up-regulation can react with superoxide anions forming peroxynitrite, thereby promoting nitrosative stress and endothelial dysfunction. In addition, abnormal iNOS activity can up-regulate arginase activity, allowing it to compete with eNOS for L-arginine, thereby resulting in reduced NO bioavailability. This may also lead to eNOS uncoupling with enhanced production of superoxide anions instead of NO. All these alterations mediated by iNOS apparently contribute to hypertension and its complications. We also reviewed current evidence showing the effects of iNOS inhibitors on different animal models of hypertension. iNOS inhibition apparently exerts antihypertensive effects, decreases oxidative and nitrosative stress, and improves vascular function. Together, these studies highlight the possibility that iNOS is a potential pharmacological target in hypertension.
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