Open AccessExcitation-contraction coupling and calcium release in atrial muscle
Author(s) -
Lothar A. Blatter,
Giedrius Kanaporis,
Elizabeth Martínez-Hernández,
Yuriana OropezaAlmazán,
Kathrin Banach
Publication year - 2021
Publication title -
pflügers archiv für die gesamte physiologie des menschen und der tiere/pflügers archiv
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.428
H-Index - 129
eISSN - 0365-267X
pISSN - 0031-6768
DOI - 10.1007/s00424-020-02506-x
Subject(s) - ryanodine receptor , biophysics , serca , endoplasmic reticulum , myocyte , depolarization , chemistry , calcium , contraction (grammar) , ryanodine receptor 2 , calcium signaling , afterdepolarization , medicine , electrophysiology , biology , repolarization , biochemistry , atpase , enzyme
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 Ca 2+ induced Ca 2+ release from the sarcoplasmic reticulum (SR) Ca 2+ 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 Ca 2+ release that assigns a novel role to the SR SERCA pump and involves a concerted "tandem" activation of the ryanodine receptor Ca 2+ release channel by cytosolic and luminal Ca 2+ . We discuss the contribution of the inositol 1,4,5-trisphosphate (IP 3 ) receptor Ca 2+ release channel as an auxiliary pathway to Ca 2+ signaling, and we review IP 3 receptor-induced Ca 2+ release involvement in beat-to-beat ECC, nuclear Ca 2+ signaling, and arrhythmogenesis. Finally, we explore the topic of electromechanical and Ca 2+ alternans and its ramifications for atrial arrhythmia.