期刊
FRONTIERS IN PHYSIOLOGY
卷 6, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2015.00028
关键词
arrhythmias; coupled-clock pacemaker system; heart rate variability; mathematical modeling; sinoatrial node
类别
资金
- Intramural Research Program of the NIH, National Institute on Aging
- Technion V.P.R Fund-Mallat Family Research Fund
- NSFC-ISF joint research program [398/14]
At the beginning of this century, debates regarding what are the main control mechanisms that ignite the action potential (AP) in heart pacemaker cells dominated the electrophysiology field. The original theory which prevailed for over 50 years had advocated that the ensemble of surface membrane ion channels (i.e., M-clock) is sufficient to ignite rhythmic APs. However, more recent experimental evidence in a variety of mammals has shown that the sarcoplasmic reticulum (SR) acts as a Ca2+-clock rhythmically discharges diastolic local Ca2+ releases (LCRs) beneath the cell surface membrane. LCRs activate an inward current (likely that of the Na/+Ca2+ exchanger) that prompts the surface membrane M-clock to ignite an AP Theoretical and experimental evidence has mounted to indicate that this clock crosstalk operates on a beat-to-beat basis and determines both the AP firing rate and rhythm. Our review is focused on the evolution of experimental definition and numerical modeling of the coupled-clock concept, on how mechanisms intrinsic to pacemaker cell determine both the heart rate and rhythm, and on future directions to develop further the coupled-clock pacemaker cell concept.
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