Zaborovskaia L D, Khodorov B I
Neirofiziologiia. 1982;14(6):636-43.
Voltage-clamp experiments on the frog Ranvier node have shown that batrachotoxin (BTX) decreases drastically the sensitivity of sodium channels to the blocking action of various tertiary (procaine, trimecaine, ajmalin, strychnine) and quaternary (QX-572, N-propylajmaline) amine drugs but does not affect noticeably sodium channels blockade produced by neutral benzocaine. The inhibition of BTX-modified sodium current by large concentrations of trimecaine (3.5 mM) is time- and voltage-dependent. Neither of the amines used proved to be able to cause frequency-dependent (cummulative) block of modified channels. Unblocking of these channels during washing of the node with Ringer solution proceeds much faster than that of normal channels. On the contrary, restoration of normal and modified currents blocked previously by benzocaine has the same time course. The relationships between "receptors" for BTX and various sodium channel blockers are discussed.
对青蛙郎飞结进行的电压钳实验表明,蟾毒素(BTX)可大幅降低钠通道对各种叔胺(普鲁卡因、三甲卡因、阿义马林、士的宁)和季胺(QX - 572、N - 丙基阿义马林)类药物阻断作用的敏感性,但对中性苯佐卡因产生的钠通道阻断作用无明显影响。高浓度三甲卡因(3.5 mM)对BTX修饰的钠电流的抑制具有时间和电压依赖性。所用的胺类均未被证明能够引起修饰通道的频率依赖性(累积性)阻断。在用林格液冲洗节点时,这些通道的去阻断过程比正常通道快得多。相反,先前被苯佐卡因阻断的正常电流和修饰电流的恢复具有相同的时间进程。文中讨论了BTX“受体”与各种钠通道阻滞剂之间的关系。