论文部分内容阅读
心肌钾离子通道分两类 ,一类是电压依赖型 ,另一类是内向整流型。前者包括瞬间外向钾通道ITO(相应与分子克隆Kv4.2 / 4.3) ,慢迟缓性钾通道IKS(KvLQT1+MinK) ,快迟缓性钾通道IKR(HERG + ?) ,超快迟缓性钾通道IKur (Kv1 5 )。去极化动作电位激活这些钾电流触发和加速细胞膜复极化。后者包括ATP -敏感性钾通道IK ,ATP(相应与分子克隆KIR6 .2+SUR2A) ,静息内向整流钾通道IK1(KIR2 .2 ?) ,乙酰胆碱 /腺苷激活性钾通道IK ,ACh或IK ,ADO(KIR3 1/ 3 4)。IK ,ATP在心肌缺氧或缺血 ,细胞内ATP/ADP比值降低时被激活 ,导致动作电位缩短 ,钙离子内流减少 ,细胞超极化 ,兴奋性降低 ,起到保护心肌的作用。IK1的主要作用是维持静息膜电位。兴奋迷走神经引起的心律减慢主要是通过激活IK ,ACh,降低窦房结自律性及房室传导。限于篇幅和作者近年的研究发现 ,本文将重点讨论心肌乙酰胆碱或腺苷激活性钾通道IK ,ACh的信息传递。目前膜限性理论 (membrane -delimitedpathway)广为接受 ,即乙酰胆碱或腺苷刺激其相应受体 (M2或A1) ,激活与其偶合的G -蛋白 ,继而产生的游离βγ双体直接与KACh蛋白结合 ,从而激活KACh通道。然而 ,新近的研究发现表明由第二信使为中介的去磷酸化酶活性增加 ,也可以激活KACh通道。此外 ,作者发现细胞
Myocardial potassium channel is divided into two categories, one is voltage-dependent, the other is inward rectification. The former included transient outward potassium channel ITO (corresponding to molecular clone Kv4.2 / 4.3), slow-onset potassium channel IKS (KvLQT1 + MinK), fast-acting potassium channel IKR (HERG +?), Ultrafast potassium channel IKur (Kv1 5). Depolarizing action potentials activate these potassium currents to trigger and accelerate cell membrane repolarization. The latter included ATP - sensitive potassium channel IK, ATP (corresponding to molecular clone KIR6 .2 + SUR2A), resting inward rectifier potassium channel IK1 (KIR2 .2?), Acetylcholine / adenosine activated potassium channel IK, ACh or IK, ADO (KIR3 1/3 4). IK, ATP is activated in hypoxia or ischemia of myocardium and the decrease of intracellular ATP / ADP ratio, resulting in shortening of action potentials, decrease of influx of calcium ions, hyperpolarization of cells, decrease of excitability and protection of myocardium. The main role of IK1 is to maintain resting membrane potential. Vagus nerve stimulation caused by slow heart rate is mainly through the activation of IK, ACh, reduce sinus node self-regulation and atrioventricular conduction. Due to limited space and the author’s recent research found that this article will focus on myocardial acetylcholine or adenosine-activated potassium channel IK, ACh of information transmission. It is now widely accepted that membrane-specific pathways, that is, acetylcholine or adenosine stimulate their respective receptors (M2 or A1), activate the G-protein to which they are coupled, and that the resulting free βγ-binders directly bind to the KACh protein , Thus activating KACh channel. However, recent studies have shown that an increase in dephosphorylase activity mediated by a second messenger can also activate KACh channels. In addition, the authors found cells