Regulation of [Ca2+](i) in canine airway smooth muscle by Ca2+-ATPase and Na+/Ca2+ exchange mechanisms
Regulation of [Ca2+](i) in canine airway smooth muscle by Ca2+-ATPase and Na+/Ca2+ exchange mechanisms
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DOI：
10.1152/ajplung.1997.273.2.l322
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发表时间：
1997-08-01
影响因子：
4.9
通讯作者：
Wattie, J
中科院分区：
文献类型：
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作者：
Janssen, LJ;Walters, DK;Wattie, J
我们使用Fura 2荧光、离子电流和收缩作为细胞内Ca 2+浓度（[Ca 2 +]（i））的指标来研究气道平滑肌（SM）中的Ca 2+处理。卡巴胆碱引起[Ca 2 +]（i）的短暂升高，其幅度较小，并且在37 ℃时衰减速度较快，表明某些温度敏感机制有助于恢复。去除外部Na+对激动剂诱发的Ca 2+瞬变或收缩或自发Ca 2+依赖性K+电流没有影响。选择性肌浆网（SR）Ca ~（2+）-ATP酶抑制剂环匹阿尼酸（Cyclopiazonic acid）可引起[Ca ~（2+）]（i）短暂升高和收缩，显著减慢胆碱能Ca ~（2+）瞬变的恢复，并使SR耗竭。钒酸钠可引起[Ca ~（2+）]（i）持续升高，显著减慢胆碱能Ca ~（2+）瞬变的衰减。我们的结论是，在犬气道SM中，1）Na+/Ca 2+交换最多只能对Ca 2+稳态做出微小贡献，2）SR Ca 2 +-ATP酶补偿自发和激动剂触发的Ca 2+释放，3）[Ca 2 +]（i）稳态涉及其他一些挤出途径，可能是质膜Ca 2 +-ATP酶。
We investigated Ca2+ handling in airway smooth muscle (SM) using fura 2 fluorescence, ion currents, and contractions as indexes of intracellular Ca2+ concentration ([Ca2+](i)). Carbachol evoked a transient elevation of [Ca2+](i), the magnitude of which was smaller and the rate of decay faster at 37 degrees C, indicating that some temperature-sensitive mechanism contributed to recovery Removal of external Na+ had no effect on agonist-evoked Ca2+ transients or contractions or on spontaneous Ca2+-dependent K+ currents. Cyclopiazonic acid, a selective inhibitor of the sarcoplasmic reticulum (SR) Ca2+-ATPase, evoked a transient elevation of [Ca2+](i) and contraction, markedly slowed recovery of the cholinergic Ca2+ transient, and depleted the SR. Sodium vanadate evoked a sustained elevation of [Ca2+](i) and markedly slowed the decay of the cholinergic Ca2+ transient. We conclude that, in canine airway SM, 1) Na+/Ca2+ exchange makes at best only minor contribution to Ca2+ homeostasis, 2) the SR Ca2+-ATPase compensates for spontaneous and agonist-triggered release of Ca2+, and 3) [Ca2+](i) homeostasis involves some other extrusion pathway, likely the plasmalemmal Ca2+-ATPase.