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.

在心肌中，兴奋-收缩耦合 (ECC) 过程描述了将动作电位诱导的肌细胞膜去极化、表面膜离子通道激活、触发 Ca ²⁺诱导的肌浆网 (SR) 释放Ca ²⁺的一系列事件。 ) Ca ²⁺储存以激活最终负责心脏泵功能的收缩机制。在这里，我们回顾心房和心室组织之间 ECC 的结构和功能属性的异同。我们探索了心房ECC和Ca ^{2+的新型“火-扩散-吸收-火”范式}释放为 SR SERCA 泵分配了新的作用，并涉及通过细胞溶质和管腔 Ca ^{2+协同“串联”激活兰尼碱受体 Ca 2+}释放通道。我们讨论了肌醇 1,4,5-三磷酸 (IP ₃ ) 受体 Ca ²⁺释放通道作为 Ca ²⁺信号传导的辅助途径的贡献，我们回顾了 IP ₃受体诱导的 Ca ²⁺释放参与节拍-跳动 ECC、核 Ca ²⁺信号传导和心律失常发生。最后，我们探讨了机电和 Ca ²⁺交替的主题及其对房性心律失常的影响。