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心房肌的兴奋-收缩偶联和钙释放。

Excitation-contraction coupling and calcium release in atrial muscle.

机构信息

Department of Physiology & Biophysics, Rush University Medical Center, 1750 W. Harrison Street, Chicago, IL, 60612, USA.

Department of Internal Medicine/Cardiology, Rush University Medical Center, Chicago, IL, 60612, USA.

出版信息

Pflugers Arch. 2021 Mar;473(3):317-329. doi: 10.1007/s00424-020-02506-x. Epub 2021 Jan 5.

DOI:10.1007/s00424-020-02506-x
PMID:33398498
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7940565/
Abstract

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 induced Ca release from the sarcoplasmic reticulum (SR) Ca 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 release that assigns a novel role to the SR SERCA pump and involves a concerted "tandem" activation of the ryanodine receptor Ca release channel by cytosolic and luminal Ca. We discuss the contribution of the inositol 1,4,5-trisphosphate (IP) receptor Ca release channel as an auxiliary pathway to Ca signaling, and we review IP receptor-induced Ca release involvement in beat-to-beat ECC, nuclear Ca signaling, and arrhythmogenesis. Finally, we explore the topic of electromechanical and Ca alternans and its ramifications for atrial arrhythmia.

摘要

在心肌中,兴奋-收缩偶联(ECC)的过程描述了将动作电位引起的心肌细胞膜去极化、表面膜离子通道激活、触发肌浆网(SR)Ca 储存中 Ca 释放引发收缩机制激活的一连串事件,最终负责心脏的泵功能。在这里,我们回顾了心房和心室组织之间 ECC 和 Ca 释放的结构和功能属性的相似之处和差异。我们探索了心房 ECC 和 Ca 释放的新型“火扩散吸收火”范例,该范例赋予了 SR SERCA 泵的新作用,并涉及细胞浆和腔 Ca 协同“串联”激活 Ryanodine 受体 Ca 释放通道。我们讨论了肌醇 1,4,5-三磷酸(IP)受体 Ca 释放通道作为 Ca 信号辅助途径的贡献,我们回顾了 IP 受体诱导的 Ca 释放在心脏跳动 ECC、核 Ca 信号和心律失常发生中的作用。最后,我们探讨了机电和 Ca 交替的主题及其对心房性心律失常的影响。

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本文引用的文献

1
Mitochondrial calcium uniporter complex activation protects against calcium alternans in atrial myocytes.线粒体钙单向转运体复合物的激活可防止心房肌细胞内钙离子震荡。
Am J Physiol Heart Circ Physiol. 2020 Oct 1;319(4):H873-H881. doi: 10.1152/ajpheart.00375.2020. Epub 2020 Aug 28.
2
Effect of carvedilol on atrial excitation-contraction coupling, Ca release, and arrhythmogenicity.卡维地洛对心房兴奋-收缩偶联、钙释放和致心律失常性的影响。
Am J Physiol Heart Circ Physiol. 2020 May 1;318(5):H1245-H1255. doi: 10.1152/ajpheart.00650.2019. Epub 2020 Apr 10.
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Action potential shortening rescues atrial calcium alternans.动作电位时程缩短可挽救心房钙波动。
J Physiol. 2019 Feb;597(3):723-740. doi: 10.1113/JP277188. Epub 2018 Dec 5.
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Long QT Syndrome: A Comprehensive Review of the Literature and Current Evidence.长 QT 综合征:文献综述及当前证据。
Curr Probl Cardiol. 2019 Mar;44(3):92-106. doi: 10.1016/j.cpcardiol.2018.04.002. Epub 2018 May 10.
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Membrane potential determines calcium alternans through modulation of SR Ca load and L-type Ca current.膜电位通过调节肌浆网钙负荷和L型钙电流来决定钙交替变化。
J Mol Cell Cardiol. 2017 Apr;105:49-58. doi: 10.1016/j.yjmcc.2017.02.004. Epub 2017 Feb 28.
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A novel mechanism of tandem activation of ryanodine receptors by cytosolic and SR luminal Ca during excitation-contraction coupling in atrial myocytes.心房肌细胞兴奋-收缩偶联过程中,胞质和肌浆网腔Ca对兰尼碱受体串联激活的新机制。
J Physiol. 2017 Jun 15;595(12):3835-3845. doi: 10.1113/JP273611. Epub 2017 Feb 1.
7
Dyssynchronous calcium removal in heart failure-induced atrial remodeling.心力衰竭所致心房重构中的钙移除不同步
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Axial tubule junctions control rapid calcium signaling in atria.轴突小管连接调控心房中的快速钙信号传导。
J Clin Invest. 2016 Oct 3;126(10):3999-4015. doi: 10.1172/JCI88241. Epub 2016 Sep 19.
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Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice.线粒体通透性转换孔(mPTP)在心律失常中的作用:来自亲环素D基因敲除小鼠的证据。
Cell Calcium. 2016 Dec;60(6):363-372. doi: 10.1016/j.ceca.2016.09.001. Epub 2016 Sep 2.
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Calcium-activated chloride current determines action potential morphology during calcium alternans in atrial myocytes.钙激活氯离子电流决定心房肌细胞钙交替期间的动作电位形态。
J Physiol. 2016 Feb 1;594(3):699-714. doi: 10.1113/JP271887. Epub 2016 Jan 15.