Ju Yue-kun, Allen David G
School of Medical Sciences (F13), University of Sydney, Sydney, NSW 2006, Australia.
Heart Lung Circ. 2007 Oct;16(5):349-55. doi: 10.1016/j.hlc.2007.07.004. Epub 2007 Sep 5.
Store-operated Ca(2+) channels (SOCCs) were first identified in non-excitable cells by the observation that depletion of Ca(2+) stores caused increased influx of extracellular Ca(2+). Recent studies have suggested that SOCCs might be related to the transient receptor potential (TRPC) gene family. The mechanism of cardiac pacemaking involves voltage-dependent pacemaker current; in addition there is growing evidence that intracellular sarcoplasmic reticulum (SR) Ca(2+) release plays an important role. In the present short review we assess preliminary evidence for Ca(2+) entry related to SR store depletion and expression of TRPCs in pacemaker tissue. These newer findings suggest that Ca(2+) entry and inward current triggered by store depletion might also contribute to the pacemaker current. Many hormones, drugs and interventions such as ischaemia and stretch, which alter Ca(2+) handling, will also modulate pacemaker firing thought their effect on SOCCs.
通过观察到细胞内钙库耗竭会导致细胞外钙离子内流增加，人们首次在非兴奋性细胞中发现了储存性钙通道（SOCCs）。最近的研究表明，SOCCs可能与瞬时受体电位（TRPC）基因家族有关。心脏起搏机制涉及电压依赖性起搏电流；此外，越来越多的证据表明，细胞内肌浆网（SR）钙释放起重要作用。在本简短综述中，我们评估了与SR钙库耗竭相关的钙离子内流以及起搏组织中TRPCs表达的初步证据。这些新发现表明，钙库耗竭引发的钙离子内流和内向电流也可能对起搏电流有贡献。许多改变钙处理的激素、药物和干预措施，如缺血和牵张，也会通过其对SOCCs的作用来调节起搏发放。
