作者: Iain D. Dukes , Martin Morad
DOI: 10.1007/BF00051017
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摘要: The mechanism of the interaction tedisamil with voltage-dependent K+ channels was studied using whole-cell and single-channel recordings in a variety species cell types. In rapid activation kinetics (Ito rat ventricular myocytes; IA mouse astroglial cells), enhanced inactivation current without significantly suppressing amplitude initial current. slower activation/inactivation kinetics, had divergent effect. On IK glial cells, which have slow were peak reduced. other hand, guinea-pig myocytes, even no inactivation, slowed or completely suppressed Finally, but (pedestal-type myocytes), accelerated affecting Thus, prime determinant blocking mode appeared to be channel; that is, channel, greater block by drug. Unitary Ito currents recorded myocytes showed induced flicker open channel prolonged time between burst openings any effect on unitary conductance. These effects modeled assuming drug bound at finite rate. appears decrease interacting uniformly state channel.