PDF(Pubmed)
Abstract：
This review paper delves into the current body of evidence, offering a thorough analysis of the impact of large-conductance Ca2+-activated K+ (BKCa or BK) channels on the electrical dynamics of the heart. Alterations in the activity of BKCa channels, responsible for the generation of the overall magnitude of Ca2+-activated K+ current at the whole-cell level, occur through allosteric mechanisms. The collaborative interplay between membrane depolarization and heightened intracellular Ca2+ ion concentrations collectively contribute to the activation of BKCa channels. Although fully developed mammalian cardiac cells do not exhibit functional expression of these ion channels, evidence suggests their presence in cardiac fibroblasts that surround and potentially establish close connections with neighboring cardiac cells. When cardiac cells form close associations with fibroblasts, the high single-ion conductance of these channels, approximately ranging from 150 to 250 pS, can result in the random depolarization of the adjacent cardiac cell membranes. While cardiac fibroblasts are typically electrically non-excitable, their prevalence within heart tissue increases, particularly in the context of aging myocardial infarction or atrial fibrillation. This augmented presence of BKCa channels\' conductance holds the potential to amplify the excitability of cardiac cell membranes through effective electrical coupling between fibroblasts and cardiomyocytes. In this scenario, this heightened excitability may contribute to the onset of cardiac arrhythmias. Moreover, it is worth noting that the substances influencing the activity of these BKCa channels might influence cardiac electrical activity as well. Taken together, the BKCa channel activity residing in cardiac fibroblasts may contribute to cardiac electrical function occurring in vivo.
摘要：
这篇综述论文深入研究了当前的证据，全面分析大电导Ca2激活的K（BKCa或BK）通道对心脏电动力学的影响。BKCa通道活性的改变，负责在全细胞水平上产生Ca2+激活的K+电流的整体大小，通过变构机制发生。膜去极化和细胞内Ca2离子浓度升高之间的协同相互作用共同促进了BKCa通道的激活。尽管完全发育的哺乳动物心脏细胞不表现出这些离子通道的功能表达，有证据表明，它们存在于围绕相邻心肌细胞并可能与之建立密切联系的心脏成纤维细胞中。当心肌细胞与成纤维细胞形成紧密的联系时，这些通道的高单离子电导，大约从150到250pS，会导致相邻心脏细胞膜的随机去极化。虽然心脏成纤维细胞通常是电不可兴奋的，它们在心脏组织中的患病率增加，特别是在老年心肌梗死或心房颤动的情况下。这种增加的BKCa通道电导的存在具有通过成纤维细胞和心肌细胞之间的有效电耦合来放大心脏细胞膜兴奋性的潜力。在这种情况下，这种增强的兴奋性可能导致心律失常的发生.此外，值得注意的是，影响这些BKCa通道活性的物质也可能影响心脏电活动。一起来看,存在于心脏成纤维细胞中的BKCa通道活性可能有助于体内发生的心脏电功能。
