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Atrial tachycardia induces remodelling of muscarinic receptors and their coupled potassium currents in canine left atrial and pulmonary vein cardiomyocytes.房性心动过速可诱导犬左心房和肺静脉心肌细胞中M胆碱能受体及其偶联的钾电流发生重塑。
Br J Pharmacol. 2007 Dec;152(7):1021-32. doi: 10.1038/sj.bjp.0707376. Epub 2007 Jul 9.
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Increased susceptibility to atrial tachyarrhythmia in spontaneously hypertensive rat hearts.自发性高血压大鼠心脏对房性快速性心律失常的易感性增加。
Hypertension. 2007 Mar;49(3):498-505. doi: 10.1161/01.HYP.0000257123.95372.ab. Epub 2007 Jan 22.
3
Atrial electrical and structural abnormalities in an ovine model of chronic blood pressure elevation after prenatal corticosteroid exposure: implications for development of atrial fibrillation.产前暴露于皮质类固醇激素后绵羊慢性血压升高模型中的心房电和结构异常：对房颤发生发展的影响
Eur Heart J. 2006 Dec;27(24):3045-56. doi: 10.1093/eurheartj/ehl360. Epub 2006 Nov 10.
4
Kir3-based inward rectifier potassium current: potential role in atrial tachycardia remodeling effects on atrial repolarization and arrhythmias.基于Kir3的内向整流钾电流：对心房复极化和心律失常的心房心动过速重塑效应中的潜在作用。
Circulation. 2006 Apr 11;113(14):1730-7. doi: 10.1161/CIRCULATIONAHA.105.561738. Epub 2006 Apr 3.
5
The G protein-gated potassium current I(K,ACh) is constitutively active in patients with chronic atrial fibrillation.G蛋白门控钾电流I（K，ACh）在慢性心房颤动患者中呈组成性激活。
Circulation. 2005 Dec 13;112(24):3697-706. doi: 10.1161/CIRCULATIONAHA.105.575332. Epub 2005 Dec 5.
6
Mechanisms of atrial fibrillation: lessons from animal models.心房颤动的机制：来自动物模型的经验教训。
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The M3 receptor-mediated K(+) current (IKM3), a G(q) protein-coupled K(+) channel.M3受体介导的钾离子电流（IKM3），一种G(q)蛋白偶联的钾离子通道。
J Biol Chem. 2004 May 21;279(21):21774-8. doi: 10.1074/jbc.C400100200. Epub 2004 Mar 31.
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Characterization of a hyperpolarization-activated time-dependent potassium current in canine cardiomyocytes from pulmonary vein myocardial sleeves and left atrium.肺静脉心肌袖和左心房犬心肌细胞中一种超极化激活的时间依赖性钾电流的特性分析
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9
Differential alterations of receptor densities of three muscarinic acetylcholine receptor subtypes and current densities of the corresponding K+ channels in canine atria with atrial fibrillation induced by experimental congestive heart failure.实验性充血性心力衰竭诱导犬心房颤动时，三种毒蕈碱型乙酰胆碱受体亚型的受体密度及相应钾通道电流密度的差异改变。
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Pulmonary vein denervation enhances long-term benefit after circumferential ablation for paroxysmal atrial fibrillation.肺静脉去神经支配可增强阵发性心房颤动环肺静脉消融术后的长期获益。
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不止一种类型：在心房颤动实验模型中，多种毒蕈碱受体偶联的钾电流发生重塑。

More types than one: multiple muscarinic receptor coupled K+ currents undergo remodelling in an experimental model of atrial fibrillation.

作者信息

James A F, Hancox J C

机构信息

Department of Physiology and Pharmacology, and Bristol Heart Institute Cardiovascular Research Laboratories, School of Medical Sciences, University of Bristol, Bristol, UK.

出版信息

Br J Pharmacol. 2007 Dec;152(7):981-3. doi: 10.1038/sj.bjp.0707437. Epub 2007 Sep 10.

DOI:10.1038/sj.bjp.0707437
PMID:17828293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2095112/
Abstract

The common cardiac arrhythmia atrial fibrillation (AF) tends to show progression in its severity, which is associated with 'remodelling': structural and electrophysiological changes that facilitate arrhythmia induction and maintenance. In this issue of the BJP, Yeh and colleagues demonstrate for the first time, down-regulation of three types of muscarinic cholinergic receptor (mAChR) coupled K+ currents (IKM2, IKM3 and IKM4) and of M2, M3 and M4 mAChR subtype proteins, in a canine model of atrial tachycardia (AT) induced remodelling. The IKMs and their extent of AT-induced remodelling were similar in left-atrial and pulmonary vein (PV) myocytes, so remodelling of M2-M4 receptor-linked currents appears not to underlie the unique contribution of PVs to AF. Parasympathetic stimulation can increase susceptibility to AF; thus remodelling of M2-M4 receptors and K+ currents could be adaptive in AT. Further work is warranted to determine whether or not remodelling of multiple mAChRs and currents also contributes to human AF.

摘要

常见的心律失常——心房颤动（AF）往往会在严重程度上表现出进展，这与“重塑”有关：即促进心律失常诱发和维持的结构及电生理变化。在本期《英国药理学杂志》中，Yeh及其同事首次证明，在犬类心房性心动过速（AT）诱导的重塑模型中，三种毒蕈碱型胆碱能受体（mAChR）偶联的钾电流（IKM2、IKM3和IKM4）以及M2、M3和M4 mAChR亚型蛋白表达下调。左心房和肺静脉（PV）心肌细胞中的IKMs及其AT诱导的重塑程度相似，因此M2 - M4受体相关电流的重塑似乎并非PVs对AF独特作用的基础。副交感神经刺激可增加对AF的易感性；因此，M2 - M4受体和钾电流的重塑在AT中可能具有适应性。有必要进一步开展研究，以确定多种mAChRs和电流的重塑是否也与人类AF有关。