Nishimura M, Asai F, Urakawa N
Jpn J Pharmacol. 1982 Apr;32(2):231-5. doi: 10.1254/jjp.32.231.
Verapamil was examined for its effect on the frequency of miniature end-plate potential (m.e.p.p.) in rat diaphragm muscles. Verapamil (5 x 10(-5) M) raised the m.e.p.p. frequency. This effect was reversible, reproducible, and concentration dependent. The rise in the frequency was maintained in the presence of external Ca++ but was transient in the absence of external Ca++. Lowering the temperature to 20 degrees C slightly decreased the average frequency of m.e.p.p. in the normal medium. The effect of verapamil was also present at a low temperature but was delayed in its onset. The resting membrane potential of the muscle fiber was not affected by the agent. These results suggest the possibility that verapamil increases the transmitter release from motor nerve terminals, and the effect is possibly due to a release of Ca++ for its initiation, but is dependent on external Ca++ for its maintenance.
研究了维拉帕米对大鼠膈肌微小终板电位(m.e.p.p.)频率的影响。维拉帕米(5×10⁻⁵ M)可提高m.e.p.p.频率。这种作用是可逆的、可重复的且浓度依赖性的。在有细胞外Ca²⁺存在时,频率升高得以维持,但在无细胞外Ca²⁺时则是短暂的。将温度降至20℃会使正常培养基中m.e.p.p.的平均频率略有降低。维拉帕米在低温时也有作用,但起效延迟。该药物不影响肌纤维的静息膜电位。这些结果提示,维拉帕米可能增加运动神经末梢的递质释放,其作用可能因Ca²⁺释放而启动,但维持则依赖于细胞外Ca²⁺。