A RAPIDLY ACTIVATING DELAYED RECTIFIER K+ CHANNEL IN RABBIT SINOATRIAL NODE CELLS

被引:57
作者
ITO, H [1 ]
ONO, K [1 ]
机构
[1] KYUSHU UNIV, FAC MED, DEPT PHYSIOL, FUKUOKA 81282, JAPAN
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1995年 / 269卷 / 02期
关键词
DELAYED RECTIFIER POTASSIUM CURRENT; CLASS III ANTIARRHYTHMIC AGENT; E-4031; SINGLE-CHANNEL RECORDING;
D O I
10.1152/ajpheart.1995.269.2.H443
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The single-channel current of the delayed rectifier K+ current (I-K) was recorded in rabbit sinoatrial node cells. In the cell-attached patch, depolarization from -70 mV to potentials more positive than -50 mV activated the I-K channel while repolarization deactivated it. The single-channel conductance was 7.8 pS for the outward current and 10.8 pS for the inward current (n = 6). The steady-state open probability (NPo) was maximum at around -30 mV and markedly decreased at more positive potentials. On repolarization from positive potentials, the channel was initially closed and then rapidly opened. The ensemble average showed an initial rise to a peak followed by the deactivation time course. Because the channel events were completely blocked by E-4031, the drug-sensitive component was examined in the whole cell current. The steady-state current-voltage relation of the drug-sensitive current showed a marked negative slope at potentials more positive than -10 mV. Upon repolarization, the drug-sensitive current initially increased (removal of inactivation) to the peak of the outward tail current, which was in agreement with the ensemble average of the single-channel current. We conclude that I-K in the sinoatrial node cells is largely composed of the rapidly activating I-K (I-K,I-r) channels and that the inward rectification of I-K,I-r, which is more marked than had been assumed in previous studies, is due to the decrease in NPo.
引用
收藏
页码:H443 / H452
页数:10
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