Oike M, Ito Y
Department of Pharmacology, Faculty of Medicine, Kyushu University, Japan.
Eur J Pharmacol. 1997 Jan 29;319(2-3):291-8. doi: 10.1016/s0014-2999(96)00846-1.
In non-excitable cells, a Ca2+ entry pathway is opened after the depletion of intracellular Ca2+ store sites. We have tried to estimate the sensitivity of this pathway to Ca2+ release using bovine aortic endothelial cells. Single application of a high concentration (30 microM) of ATP released almost all stored Ca2+ in Ca(2+)-free extracellular solution, whereas a low concentration of ATP (30 nM) produced a partial (57.3 +/- 3.0%) release of Ca2+. By 10 min of Ca2+ re-perfusion, the Ca2+ store site was reloaded to 97.1% of its initial filling state. When thapsigargin was applied to this cell in Mn2+ solution, Mn(2+)-induced quenching of fura-2 dye started when 19.3 +/- 5.3% of Ca2+ release, produced by 30 nM ATP, had occurred. Therefore, Ca2+ release required for Mn2+ entry was estimated as 11.1 +/- 3.0% of stored Ca2+. These results indicate that intracellular Ca2+ concentration is controlled dynamically by simultaneously occurring Ca2+ release and entry in bovine aortic endothelial cells.
在非兴奋性细胞中，细胞内钙储存位点耗尽后会开启一条钙离子内流途径。我们试图利用牛主动脉内皮细胞来评估该途径对钙释放的敏感性。在无钙的细胞外溶液中单次施加高浓度（30微摩尔）的ATP几乎释放了所有储存的钙离子，而低浓度的ATP（30纳摩尔）则使钙离子产生了部分（57.3±3.0%）释放。经过10分钟的钙再灌注，钙储存位点重新加载至其初始填充状态的97.1%。当在锰离子溶液中对该细胞施加毒胡萝卜素时，在由30纳摩尔ATP产生的19.3±5.3%的钙释放发生时，锰离子诱导的fura-2染料淬灭开始。因此，锰离子内流所需的钙释放量估计为储存钙的11.1±3.0%。这些结果表明，在牛主动脉内皮细胞中，细胞内钙离子浓度通过同时发生的钙释放和内流而受到动态控制。
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