Satoh H, Hashimoto K
Eur J Pharmacol. 1986 Feb 18;121(2):211-9. doi: 10.1016/0014-2999(86)90492-9.
Electrophysiological effects of alinidine on rabbit sino-atrial node cells were examined. Alinidine was applied in concentrations between 0.3 and 100 micrograms/ml and decreased the spontaneous frequency in a dose-dependent manner. The maximum rate of rise and the amplitude of action potentials of the spontaneously beating rabbit sino-atrial node were decreased in the presence of alinidine concentrations higher than 10 and 100 micrograms/ml, respectively. The maximum diastolic potential was depolarized by alinidine at 100 micrograms/ml. The main effect of alinidine was a dose-dependent decrease in slope of diastolic depolarization (a prolongation of the cycle length) and a delayed repolarization of the action potential. In voltage clamp experiments, alinidine suppressed the slow inward current (Is) and the outward current (Ik) dose dependently, without altering steady-state inactivation of Is (f infinity) and the activation of Ik (p infinity). The hyperpolarization-activated inward current (Ih) was also reduced. These results suggested that alinidine decreased Is, Ik and Ih due to reduction in the conductance of these current systems. The changes in the ionic currents in the presence of alinidine can explain the changes in configuration of the action potential and must contribute to the negative chronotropic action of alinidine.
研究了阿利尼定对兔窦房结细胞的电生理效应。阿利尼定的应用浓度为0.3至100微克/毫升，其以剂量依赖性方式降低自发频率。在阿利尼定浓度分别高于10和100微克/毫升时，自发搏动的兔窦房结动作电位的最大上升速率和幅度降低。在100微克/毫升的阿利尼定作用下，最大舒张电位发生去极化。阿利尼定的主要作用是剂量依赖性地降低舒张期去极化斜率（周期长度延长）和动作电位复极化延迟。在电压钳实验中，阿利尼定剂量依赖性地抑制慢内向电流（Is）和外向电流（Ik），而不改变Is的稳态失活（f无穷大）和Ik的激活（p无穷大）。超极化激活的内向电流（Ih）也降低。这些结果表明，由于这些电流系统的电导降低，阿利尼定降低了Is、Ik和Ih。阿利尼定存在时离子电流的变化可以解释动作电位形态的变化，并且必定有助于阿利尼定的负性变时作用。
