INVESTIGATION OF THERAPEUTIC TARGET MOLECULES FOR ATRIAL FIBRILLATION REGULATING ELECTRICAL EXCITATION IN PULMONARY VEIN

为了阐明肺静脉（PV）的电生理特性，我们评估了其电活动和对影响细胞内Ca^<2+>浓度或离子通道功能的药物的反应，并将其与心房的电生理特性进行了比较。在本研究中，训练刺激在PV中诱导了触发活动，而在左心房中没有观察到。据推测，PV心肌细胞的负静息膜电位较少，在训练刺激期间诱导Ca^<2+>过载，导致触发活性的产生。毒蕈碱受体或GIRK通道的激活可以使PV的静息膜电位超极化，可能成为强烈抑制触发活性产生的药物分子靶点。

To clarify electrophysiological properties of the pulmonary vein(PV), we assessed its electrical activity and responses to drugs affecting intracellular Ca^<2+> concentration or ion-channel functions, which were compared with those in the atrium. In this study, triggered activity was induced by train stimulation in the PV, which was not observed in the left atrium. It is presumed that the less negative resting membrane potential in the PV cardiomyocytes induced Ca^<2+> overload during train stimulation, leading to generation of triggered activity. Activation of muscarinic receptors or GIRK channels, which could hyperpolarize the resting membrane potential of the PV, may become a pharmaceutical molecular target for strong suppression of the generation of triggered activity.