He Yusong, Xiao Junjie, Yang Yiqing, Zhou Qinshu, Zhang Zhimin, Pan Qin, Liu Yi, Chen Yihan
Department of Cardiology, Tongji Hospital, Tongji University, Shanghai 200065, China.
Biochem Biophys Res Commun. 2006 Dec 15;351(2):462-7. doi: 10.1016/j.bbrc.2006.10.049. Epub 2006 Oct 17.
The inward rectifier potassium channel, Kir2.1, contributes to the I(K1) current in cardiac myocytes and is closely associated with atrial fibrillation. Strong evidences have shown that atrial dilatation or stretch may result in atrial fibrillation. However, the role of Kir2.1 channels in the stretch-mediated atrial fibrillation is not clear. In this study, we constructed the recombinant plasmid of KCNJ2 that encodes the Kir2.1 channel and expressed it in CHO-K1 cells. We recorded I(K1) currents using the whole-cell patch clamping technique. Our data showed that I(K1) currents were significantly larger under stretch in the hypotonic solution than under non-stretch in the iso-osmotic solution, and the activation kinetics of the Kir2.1 channel were changed markedly by stretch as well. Thus, atrial stretch in human heart might result in excessive I(K1) currents, which is likely to increase the resting membrane potential and decrease the effective refractory period, to initiate and/or maintain atrial fibrillation.
内向整流钾通道Kir2.1对心肌细胞的I(K1)电流有贡献，且与心房颤动密切相关。有力证据表明心房扩张或拉伸可能导致心房颤动。然而，Kir2.1通道在拉伸介导的心房颤动中的作用尚不清楚。在本研究中，我们构建了编码Kir2.1通道的KCNJ2重组质粒，并在CHO-K1细胞中进行表达。我们使用全细胞膜片钳技术记录I(K1)电流。我们的数据表明，在低渗溶液中拉伸时的I(K1)电流显著大于等渗溶液中未拉伸时的I(K1)电流，并且拉伸也显著改变了Kir2.1通道的激活动力学。因此，人体心脏中的心房拉伸可能导致I(K1)电流过大，这可能会增加静息膜电位并缩短有效不应期，从而引发和/或维持心房颤动。
