肌浆网内钙容量减少对心肌细胞钙释放的影响

目的:较系统地研究肌浆网(SR)内钙容量的减少对心肌细胞钙释放的影响.方法:采用肌浆网膜的钙泵抑制剂thapsigargin(TG)耗减SR内钙容量,以喷咖啡因的方法估测SR内钙容量,以局部场刺激的方法诱发全细胞的钙释放.胞内钙信号的变化均采用激光共聚焦显微镜的方法记录.结果:SR钙泵抑制剂TG以剂量依赖和非线性的时间依赖方式引致心肌细胞SR内钙容量的耗减,而钙容量的耗减可相应地引起全细胞水平的钙释放减少.但二者的变化不完全平行,SR内钙容量的少量减少即可引起胞内钙释放的显著减少,而当SR内钙耗减到一定程度后(虽然此时SR内Ca2 仍远高于胞质内钙),场刺激已很难或无法引致钙释放.结论:心肌细胞SR内钙容量对胞内钙释放具有重要的非线性调节作用.

Regulation of sarcoplasmic reticulum Ca2+ content depletion on cardiac Ca2+release

AIM: To systematically investigate the effects of sarcoplasmic reticulum (SR) Ca~(2+) content depletion on cardiac Ca~(2+) release. METHODS: Thapsigargin, a potent SR Ca~(2+) pump inhibitor, was used to deplete the SR Ca~(2+) content. The SR Ca~(2+) content was estimated by traditional caffeine puff. The global Ca~(2+) release was evoked by local field stimulation and the intracellular Ca~(2+) signal was recorded by the laser scanning confocal microscope. RESULTS: The results showed that thapsigargin decreased the SR Ca~(2+) content in a dose-dependent and nonlinear time-dependent manner. The intracellular Ca~(2+) release decreased with the depletion of SR Ca~(2+). But these two decreases were not parallel to each other. A slight depletion of SR Ca~(2+) could lead to a significant decrease of Ca~(2+) release. When SR Ca~(2+) depleted to a certain degree (though still much higher Ca~(2+) in SR than in plasma), only little or no Ca~(2+) release could be triggered by field stimulation. CONCLUSION: The results suggest that SR Ca~(2+) content has some important nonlinear regulatory effect on intracellular Ca~(2+ )release.