Store-operated Ca2+ entry and TRPC expression; possible roles in cardiac pacemaker tissue.
Heart Lung Circ
; 16(5): 349-55, 2007 Oct.
Article
in En
| MEDLINE
| ID: mdl-17822952
ABSTRACT
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.
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Database:
MEDLINE
Main subject:
Sinoatrial Node
/
Biological Clocks
/
Calcium
/
Transient Receptor Potential Channels
/
Myocardial Contraction
Type of study:
Prognostic_studies
Limits:
Animals
/
Humans
Language:
En
Journal:
Heart Lung Circ
Journal subject:
ANGIOLOGIA
/
CARDIOLOGIA
Year:
2007
Type:
Article
Affiliation country:
Australia