Excitation-contraction coupling and calcium release in atrial muscle

被引:17
作者
Blatter, L. A. [1 ]
Kanaporis, G. [1 ]
Martinez-Hernandez, E. [1 ]
Oropeza-Almazan, Y. [1 ]
Banach, K. [2 ]
机构
[1] Rush Univ, Med Ctr, Dept Physiol & Biophys, 1750 W Harrison St, Chicago, IL 60612 USA
[2] Rush Univ, Med Ctr, Dept Internal Med Cardiol, Chicago, IL 60612 USA
来源
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 2021年 / 473卷 / 03期
基金
美国国家卫生研究院;
关键词
Excitation-contraction coupling; Atrium; Ca2+ release; IP3 receptor Ca2+ signaling; Alternans; Arrhythmia; RETICULUM CA2+ RELEASE; CARDIAC RYANODINE RECEPTOR; ACTION-POTENTIAL ALTERNANS; T-WAVE ALTERNANS; SARCOPLASMIC-RETICULUM; REPOLARIZATION ALTERNANS; INTRACELLULAR CALCIUM; LUMINAL CA2+; VENTRICULAR MYOCYTES; MECHANISM;
D O I
10.1007/s00424-020-02506-x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
In cardiac muscle, the process of excitation-contraction coupling (ECC) describes the chain of events that links action potential induced myocyte membrane depolarization, surface membrane ion channel activation, triggering of Ca2+ induced Ca2+ release from the sarcoplasmic reticulum (SR) Ca2+ store to activation of the contractile machinery that is ultimately responsible for the pump function of the heart. Here we review similarities and differences of structural and functional attributes of ECC between atrial and ventricular tissue. We explore a novel "fire-diffuse-uptake-fire" paradigm of atrial ECC and Ca2+ release that assigns a novel role to the SR SERCA pump and involves a concerted "tandem" activation of the ryanodine receptor Ca2+ release channel by cytosolic and luminal Ca2+. We discuss the contribution of the inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ release channel as an auxiliary pathway to Ca2+ signaling, and we review IP3 receptor-induced Ca2+ release involvement in beat-to-beat ECC, nuclear Ca2+ signaling, and arrhythmogenesis. Finally, we explore the topic of electromechanical and Ca2+ alternans and its ramifications for atrial arrhythmia.
引用
收藏
页码:317 / 329
页数:13
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