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Negative-Feedback Regulation of ATP Release During Ischemia in Cardiac Myocytes

机译:心肌细胞缺血期间ATP释放的负反馈调控

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Extracellular ATP acts as a potent agonist on cardiomyocytes, inducing a broad range of physiological responses via P2 purinoceptors. Its concentration in the interstitial space within the heart is elevated during ischemia or hy poxia due to its release from a number of cell types, including cardiomyocytes. However, the exact mechanism responsible for the release of ATP from cardiomyocytes during ischemia is not known. In this study, we investigated whether and how the release of ATP was strictly regulated during ischemia in cultured neonatal rat cardiomyocytes. Here we show the possibility that the release of ATP from cardiomyocytes was strictly regulated during ischemia by negative-feedback mechanisms; that is, maxi-anion channel-derived ATP-induced suppression of ATP release via hemichannels in cardiomyocytes.
机译:细胞外ATP充当心肌细胞上的有效激动剂,通过P2嘌呤受体诱导广泛的生理反应。由于缺血或缺氧时它从多种细胞类型(包括心肌细胞)中释放出来,因此其在心脏内间隙中的浓度会升高。但是,尚不清楚导致缺血期间心肌细胞释放ATP的确切机制。在这项研究中,我们调查了在培养的新生大鼠心肌细胞缺血期间是否严格控制ATP的释放,以及如何对其进行严格调控。在这里,我们显示了在缺血期间,通过负反馈机制严格控制了心肌细胞中ATP的释放的可能性。也就是说,最大阴离子通道衍生的ATP通过心肌细胞中的半通道抑制了ATP的释放。

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