Carmeliet E
Laboratory of Physiology, University of Leuven, Belgium.
Fundam Clin Pharmacol. 1993;7(1):19-28. doi: 10.1111/j.1472-8206.1993.tb00214.x.
K+ channels form a large family, in which voltage-operated and ligand-operated channels can be distinguished. Under physiological conditions, four K+ currents contribute to the repolarization process and their role is discussed: i) the transient outward current (ito) is responsible for the rapid initial repolarization process from the crest of the action potential to the plateau level; ii) the delayed K+ current (iK) is involved in the overall repolarization process during the plateau; iii) the inward rectifier (iK1) is responsible for the final rapid repolarization and the maintenance of the resting potential; iv) a ligand-operated channel activated by acetylcholine and adenosine participates in the repolarization process and the maintenance of the resting potential in nodal, atrial and Purkinje cells. In the context of antiarrhythmic interventions, block of outward K+ current and prolongation of refractoriness is currently considered as an alternative to block of the Na+ current and reduction of conduction velocity. Although some of these drugs show use-dependent block, the frequency-dependent changes in current and action potential duration are not ideal.
钾离子通道构成一个大家族，其中可区分出电压门控通道和配体门控通道。在生理条件下，四种钾离子电流参与复极化过程，其作用如下：i）瞬时外向电流（ito）负责动作电位峰至平台期的快速初始复极化过程；ii）延迟钾电流（iK）参与平台期的整体复极化过程；iii）内向整流器（iK1）负责最终的快速复极化及静息电位的维持；iv）一种由乙酰胆碱和腺苷激活的配体门控通道参与结细胞、心房细胞和浦肯野细胞的复极化过程及静息电位的维持。在抗心律失常干预的背景下，目前认为阻断外向钾电流和延长不应期是阻断钠离子电流和降低传导速度的一种替代方法。尽管其中一些药物表现出使用依赖性阻断，但电流和动作电位时程的频率依赖性变化并不理想。
