Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction
Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction
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DOI：
10.1152/ajplung.2001.280.5.l870
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发表时间：
2001-05-01
影响因子：
4.9
通讯作者：
Yuan, JXJ
中科院分区：
文献类型：
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作者：
McDaniel, SS;Platoshyn, O;Yuan, JXJ
激动剂诱导的肺动脉（PA）平滑肌细胞（SMC）胞浆Ca 2+浓度（[Ca 2 +]（cyt））的增加包括从胞内储存的瞬时Ca 2+释放，随后是持续的Ca 2+内流。细胞内Ca 2+库的耗尽触发了容量性Ca 2+内流（CCE），这有助于[Ca 2 +]（cyt）的持续增加和Ca 2+重新填充到库中。在孤立的PA灌流无Ca 2+的解决方案，苯肾上腺素引起短暂的收缩，显然是由上升的[Ca 2 +]（细胞色素）由于从细胞内的钙释放存储。短暂收缩持续3-4分钟，直到Ca 2+库耗尽。恢复细胞外Ca 2+在酚妥拉明的存在下产生的收缩可能是由于[Ca 2 +]（细胞色素）通过CCE的上升。钙池操纵的钙通道阻断剂Ni ~（2+）可降低钙池耗竭激活的钙电流，降低CCE，抑制CCE介导的收缩。在单个PASMCs，我们确定，使用RT-PCR，5瞬时受体电位基因转录。这些结果表明，CCE，潜在地通过瞬时受体电位编码的Ca 2+通道，在激动剂介导的PA收缩中起着重要作用。
Agonist-induced increases in cytosolic Ca2+ concentration ([Ca2+](cyt)) in pulmonary artery (PA) smooth muscle cells (SMCs) consist of a transient Ca2+ release from intracellular stores followed by a sustained Ca2+ influx. Depletion of intracellular Ca2+ stores triggers capacitative Ca2+ entry (CCE), which contributes to the sustained increase in [Ca2+](cyt) and the refilling of Ca2+ into the stores. In isolated PAs superfused with Ca2+-free solution, phenylephrine induced a transient contraction, apparently by a rise in [Ca2+](cyt) due to Ca2+ release from the intracellular stores. The transient contraction lasted for 3-4 min until the Ca2+ store was depleted. Restoration of extracellular Ca2+ in the presence of phentolamine produced a contraction potentially due to a rise in [Ca2+](cyt) via CCE. The store-operated Ca2+ channel blocker Ni2+ reduced the store depletion-activated Ca2+ currents, decreased CCE, and inhibited the CCE-mediated contraction. In single PASMCs, we identified, using RT-PCR, five transient receptor potential gene transcripts. These results suggest that CCE, potentially through transient receptor potential-encoded Ca2+ channels, plays an important role in agonist-mediated PA contraction.