Store-Operated Ca2+ Entry and TRPC Expression; Possible Roles in Cardiac Pacemaker Tissue
| Autor: | David G. Allen, Yue-Kun Ju |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Pulmonary and Respiratory Medicine
medicine.medical_specialty medicine.medical_treatment Cardiac pacemaker Transient receptor potential channel Pacemaker potential Transient Receptor Potential Channels Biological Clocks Internal medicine medicine Extracellular Animals Humans TRPC Sinoatrial Node Sinoatrial node business.industry Endoplasmic reticulum Myocardial Contraction Cell biology Endocrinology medicine.anatomical_structure Calcium Cardiology and Cardiovascular Medicine business Intracellular |
| Zdroj: | Heart, Lung and Circulation. 16:349-355 |
| ISSN: | 1443-9506 |
| DOI: | 10.1016/j.hlc.2007.07.004 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect