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首页> 外文期刊>European Journal of Pharmacology: An International Journal >ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide.
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ATP release by cardiac myocytes in a simulated ischaemia model: inhibition by a connexin mimetic and enhancement by an antiarrhythmic peptide.

机译：在模拟的缺血模型中，心肌细胞的ATP释放：通过连接蛋白模拟物抑制和通过抗心律不齐肽增强。

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摘要

We studied the role of connexin hemichannels in the release of ATP by neonatal cardiac myocytes subject to ischaemic stress. Mechanical, osmotic and oxidative stress and changes in extracellular or intracellular Ca(2+) levels induce connexin hemichannels located in the plasma membrane to open and release small ions and molecules with signaling potential such as ATP. Since ATP release has been implicated in adaptation to oxygen deprivation, we studied its release by cardiac myocytes incubated in a custom-built hypoxia chamber for various periods. In a simulated ischaemia model (0.5% oxygen and 0.2 g/l glucose) a peak of ATP release occurred at 80 min followed by a return to steady state levels for a further 200 min. This peak of ATP release was not observed in myocytes subject to hypoxia (0.5% oxygen, 3.0 g/l glucose). ATP release in ischaemia was influenced by two classes of reagents that target connexins, the channel forming proteins of gap junctions. First, the connexin hemichannel inhibitors Gap 26 and 18a glycyrrhetinic acid abolished the ATP peak of release. Second, the AAP10, a peptide with antiarrhythmic properties markedly increased the peak of ATP release observed at 80 min of ischaemia and also induced a second smaller peak at 180-240 min. ATP content of the myocytes and Cx43 phosphorylation were monitored. Since the release of ATP in ischaemia was abolished by connexin channel inhibitors and stimulated by a peptide developed to target connexins in the context of cardiac arrhythmia, the results suggest that nucleotide release by connexin hemichannels is likely to feature in the response of myocytes to ischaemic stress in the heart.
机译：我们研究了连接蛋白半通道在缺血性应激导致的新生心肌细胞释放ATP中的作用。机械，渗透和氧化应激和细胞外或细胞内Ca（2+）水平的变化诱导位于质膜上的连接蛋白半通道打开并释放具有信号潜能的小离子和分子，例如ATP。由于ATP的释放与氧缺乏的适应有关，因此我们研究了在定制的缺氧室中孵育不同时间的心肌细胞对ATP释放的影响。在模拟的局部缺血模型（0.5％的氧气和0.2 g / l的葡萄糖）中，ATP释放的峰值出现在80分钟，然后又回到稳态水平200分钟。在遭受缺氧的心肌细胞（0.5％氧气，3.0 g / l葡萄糖）中未观察到该ATP释放峰。缺血中的ATP释放受到两类针对连接蛋白（间隙连接的通道形成蛋白）的试剂的影响。首先，连接蛋白半通道抑制剂Gap 26和18a甘草次酸消除了ATP释放峰。其次，具有抗心律失常特性的肽AAP10显着增加了缺血80分钟时观察到的ATP释放峰，并在180-240分钟时诱导了另一个较小的峰。监测心肌细胞的ATP含量和Cx43磷酸化。由于缺血性心律失常中ATP的释放被连接蛋白通道抑制剂取消，并被开发成靶向连接蛋白的肽刺激，在心律不齐的情况下，结果提示连接蛋白半通道释放的核苷酸可能是心肌细胞对缺血性应激的反应在心里。

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