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Possible Involvement of Nitric Oxide in the Suppression of the Release of Cellular ATP During Ischemia in Cultured Cardiac Myocytes

机译:一氧化氮在培养的心肌细胞缺血期间抑制一氧化氮的可能参与

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Nitric oxide (NO) plays various functional and pathological roles as an intracellular or intercellular messenger in the heart. In this study, we investigated whether NO produced during ischemia is crucially involved in the suppression of the ischemia-induced release of intracellular ATP. The concentration of extracellular ATP during ischemia was significantly increased by treatment of cultures with L-NMMA and the increase was reversed by co-treatment with SNAP, but not with decomposed SNAP, suggesting that NO suppressed the release of cellular ATP during ischemia. The L-NMMA-in-duced increase of extracellular ATP was also suppressed by treatment with blockers of connexin hemi-channels. The present results suggested that NO produced during ischemia suppressed the ischemia-induced release of intracellular ATP to the extracellular space via connexin hemichannels in cardiac myocytes.
机译:一氧化氮(NO)在心脏中发挥各种功能性和病理作用作为细胞内或细胞间信使。在这项研究中,我们研究了在缺血期间是否产生的缺血在抑制缺血诱导的细胞内ATP释放中。通过用L-NMMA治疗培养物在缺血期间细胞外ATP的浓度显着增加,并且通过用SNAP治疗而逆转,但不具有分解的捕获,表明在缺血期间不抑制细胞ATP的释放。通过用Connexin Hemi-通道的阻断剂处理,还抑制了L-NMMA型ATP的增加。本结果表明,在缺血期间没有产生的缺血诱导的缺血诱导的细胞内ATP释放到细胞外空间通过心肌细胞的血管瘤。

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