Kurihara S
Jpn J Physiol. 1975;25(6):775-88. doi: 10.2170/jjphysiol.25.775.
Procaine (1-15 mM) enhanced the spontaneous contractions of the urinary bladder smooth muscle. When a low concentration of procaine was added to normal Krebs solutions, spontaneous rhythmic contractions were enhanced. On increasing the concentration of procaine, a rise in tone (resting tension) of the preparation was observed and gradually decreased with time. The action of procaine of enhancing spontaneous contraction was observed in Na-deficient (sucrose substitutiona) and Na-free (Tris substitution) Krebs solutions. Tetrodotoxin (3 X 10(-7) G/M) DID NOT INHIBIT THE EFFECT OFPROCAINE ON MECHANICAL RESPONSE. In normal Krebs solution, procaine depolarized the membrane and increased spike frequency. The peak potential of the spike increased at 1 mM of procaine, but was suppressed at concentrations of more than 5mM. After-hyperpolization of the spike was diminished by procaine and spike duration was prolonged. The maximum rate of rise of the spike was increased immediately after application of 1 mM of procaine, but decreased wiith time. The maximum rate of fall of the spike was markedly decreased by procaine. Relative membrane resistance was increased by the application of procaine. From these results it is suggested thatprocaine mainly reduces K conductance and causes depolarization, and that enhanced spontaneous contractions are caused by depolarization and increased spike activity.
普鲁卡因(1 - 15毫摩尔)增强了膀胱平滑肌的自发收缩。当向正常的 Krebs 溶液中加入低浓度的普鲁卡因时,自发节律性收缩增强。随着普鲁卡因浓度的增加,观察到标本的张力(静息张力)升高,并随时间逐渐降低。在缺钠(蔗糖替代)和无钠(Tris 替代)的 Krebs 溶液中也观察到了普鲁卡因增强自发收缩的作用。河豚毒素(3×10⁻⁷克/毫升)并未抑制普鲁卡因对机械反应的作用。在正常的 Krebs 溶液中,普鲁卡因使膜去极化并增加了动作电位频率。在1毫摩尔普鲁卡因时动作电位的峰值增加,但在浓度超过5毫摩尔时受到抑制。普鲁卡因使动作电位后的超极化减弱,动作电位持续时间延长。在应用1毫摩尔普鲁卡因后,动作电位的最大上升速率立即增加,但随时间降低。普鲁卡因使动作电位的最大下降速率明显降低。应用普鲁卡因后相对膜电阻增加。从这些结果表明,普鲁卡因主要降低钾电导并导致去极化,增强的自发收缩是由去极化和增加的动作电位活动引起的。