| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2921431 | Heart, Lung and Circulation | 2007 | 7 Pages |
Store-operated Ca2+ channels (SOCCs) were first identified in non-excitable cells by the observation that depletion of Ca2+ stores caused increased influx of extracellular Ca2+. 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) Ca2+ release plays an important role. In the present short review we assess preliminary evidence for Ca2+ entry related to SR store depletion and expression of TRPCs in pacemaker tissue. These newer findings suggest that Ca2+ 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 Ca2+ handling, will also modulate pacemaker firing thought their effect on SOCCs.
