Store-operated Ca2+ entry and TRPC expression; possible roles in cardiac pacemaker tissue.
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.
Ju
Yue-kun
YK
School of Medical Sciences (F13), University of Sydney, Sydney, NSW 2006, Australia. ju@physio.usyd.edu.au
Allen
David G
DG
D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D012849:Sinoatrial Node / Q000502:physiology*; D050051:Transient Receptor Potential Channels / Q000502:physiology*