抄録
Ethanol intake is well known as a predisposing factor for atrial fibrillation. While recent studies identified that abnormail automaticity in pulmonary vein triggers the onset of atrial arrhythmias. However, the underlying mechanism is unknown. To investigate whether low-voltage activated T-type Ca2+ channel remodeling is involved in the ethanol insult to myocytes, we performed the whole-cell patch-clamp studies targeted on the CaV3.1 and CaV3.2 T-type Ca2+ channels expressed in the HEK293 cells. Long-time exposure of ethanol (0%, 0.1%, 0.5% and 1%) to HEK293 cells did not modify current density of CaV3.1. Meanwhile, the current density of CaV3.2 was augmented by ethanol in a dose-dependent manner; 19.8% in 0.1% ethanol, 33.1% in 0.5% ethanol, and 35.5% in 1% ethanol, respectively. These results suggest that augmentation of CaV3.2 channel current caused by ethanol exposure may promote the pacemaker potentials, triggering abnormal automaticity in pulmonary vein and/or atrial myocytes. [J Physiol Sci. 2007;57 Suppl:S79]
