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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Neuronal nitric oxide synthase negatively regulates xanthine oxidoreductase inhibition of cardiac excitation-contraction coupling.
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Neuronal nitric oxide synthase negatively regulates xanthine oxidoreductase inhibition of cardiac excitation-contraction coupling.

机译：神经元一氧化氮合酶负调节黄嘌呤氧化还原酶抑制心脏兴奋-收缩耦合。

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摘要

Although interactions between superoxide (O(2)(.-)) and nitric oxide underlie many physiologic and pathophysiologic processes, regulation of this crosstalk at the enzymatic level is poorly understood. Here, we demonstrate that xanthine oxidoreductase (XOR), a prototypic superoxide O(2)(.-) -producing enzyme, and neuronal nitric oxide synthase (NOS1) coimmunoprecipitate and colocalize in the sarcoplasmic reticulum of cardiac myocytes. Deficiency of NOS1 (but not endothelial NOS, NOS3) leads to profound increases in XOR-mediated O(2)(.-) production, which in turn depresses myocardial excitation-contraction coupling in a manner reversible by XOR inhibition with allopurinol. These data demonstrate a unique interaction between a nitric oxide and an O(2)(.-) -generating enzyme that accounts for crosstalk between these signaling pathways; these findings demonstrate a direct antioxidant mechanism for NOS1 and have pathophysiologic implications for the growing number of disease states in which increased XOR activity plays a role.
机译：虽然超氧化物（O（2）（.-））和一氧化氮之间的相互作用是许多生理和病理生理过程的基础，但对这种串扰在酶水平上的调控了解甚少。在这里，我们证明黄嘌呤氧化还原酶（XOR），原型超氧化物O（2）（.-）生产酶和神经元一氧化氮合酶（NOS1）coimmunoprecipitate和共定位在心肌细胞的肌质网中。 NOS1（但不是内皮型NOS，NOS3）的缺乏导致XOR介导的O（2）（.-）生产的大幅增加，进而以与异嘌呤醇XOR抑制可逆的方式抑制了心肌的兴奋-收缩耦合。这些数据表明一氧化氮和O（2）（.-）生成酶之间的独特相互作用，这些相互作用解释了这些信号传导途径之间的串扰。这些发现证明了NOS1的直接抗氧化机制，并且对越来越多的XOR活性起作用的疾病状态具有病理生理意义。

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