Stretch-induced alterations of human Kir2.1 channel currents.
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.
He
Yusong
Y
Department of Cardiology, Tongji Hospital, Tongji University, Shanghai 200065, China.
Xiao
Junjie
J
Yang
Yiqing
Y
Zhou
Qinshu
Q
Zhang
Zhimin
Z
Pan
Qin
Q
Liu
Yi
Y
Chen
Yihan
Y
D000818:Animals; D016466:CHO Cells; D048430:Cell Shape / Q000502:physiology*; D003001:Cloning, Molecular; D006224:Cricetinae; D003412:Cricetulus; D015640:Ion Channel Gating; D007700:Kinetics; D008564:Membrane Potentials; D009997:Osmotic Pressure; D018408:Patch-Clamp Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000502:physiology*; D013314:Stress, Mechanical
C489457:KCNJ2 protein, human; D024661:Potassium Channels, Inwardly Rectifying