Luk H N, Carmeliet E
Laboratory of Physiology, University of Leuven, Belgium.
Pflugers Arch. 1990 Aug;416(6):766-8. doi: 10.1007/BF00370627.
The Na(+)-activated K+ current was studied in inside-out patches and in whole cells isolated from the guinea-pig cardiac ventricle. The single channel conductance showed inward rectification for K+i less than K+e, but outward rectification for K+i greater than K+e. The open probability was dependent on Na+i and Na+,K(+)-pump activity. In the presence of pump blockade the channel remained active at low Na+i. Similar results were obtained in whole cells. These results suggest the existence of Na+ gradients depending on Na+,K(+)-pump activity and passive inward leak of Na+. The channel and whole cell current were blocked by R56865. The drug did not change the single channel conductance but markedly reduced open probability by shortening burst duration. The current may play an important role in action potential shortening during pump blockade.
在豚鼠心室分离出的内面向外膜片和全细胞中研究了Na(+)-激活的K+电流。单通道电导在K+i小于K+e时表现为内向整流,而在K+i大于K+e时表现为外向整流。开放概率取决于Na+i和Na+,K(+)-泵活性。在泵被阻断的情况下,通道在低Na+i时仍保持活性。在全细胞中也得到了类似的结果。这些结果表明存在依赖于Na+,K(+)-泵活性和Na+被动内向泄漏的Na+梯度。通道电流和全细胞电流被R56865阻断。该药物不改变单通道电导,但通过缩短爆发持续时间显著降低开放概率。该电流可能在泵阻断期间动作电位缩短中起重要作用。