Ito Y, Suzuki H, Kuriyama H
Jpn J Physiol. 1977;27(4):467-81. doi: 10.2170/jjphysiol.27.467.
Effects of caffeine and procaine on the membrane and mechanical properties of the smooth muscles of the rabbit main pulmonary artery were investigated using microelectrode and voltage clamp methods. Caffeine (greater than 0.5 mM) depolarized the membrane and increased ionic conductance. On the other hand, procaine (greater than 2.5 mM) depolarized the membrane, generated spikes and reduced the ionic conductance of the membrane. When depolarization-contraction relations were observed, the threshold depolarization to evoke contraction and the amplitude of the contraction were not affected by 5 mM procaine. However, the mechanical threshold was raised and the mechanical response was suppressed by treatment with 5 and 10 mM caffeine or 10 mM procaine. Procaine and caffeine accelerated the depletion of Ca++ from the stored sites of Ca-free (EGTA) solution, and suppressed the mechanical responses induced by chemical stimulation. Caffeine and procaine suppressed the increase in ionic conductance and depolarization produced by noradrenaline or prostaglandin F2alpha. Caffeine also suppressed the mechanical response induced by the above agents. Procaine suppressed the noradrenaline induced contraction, but accelerated the prostaglandin F2alpha induced contraction. From the above results, it is concluded that caffeine and procaine act not only on Ca-stored sites in the cell but also on the surface membrane. The actions of these agents were not competitive with each other, thus suggesting that the properties of the internal membrane structures, which is assumed to be a main Ca-storage site, are not exactly the same as those in striated muscles.
采用微电极和电压钳方法，研究了咖啡因和普鲁卡因对兔主肺动脉平滑肌膜及力学特性的影响。咖啡因（大于0.5 mM）使膜去极化并增加离子电导。另一方面，普鲁卡因（大于2.5 mM）使膜去极化，产生锋电位并降低膜的离子电导。观察去极化-收缩关系时，5 mM普鲁卡因不影响诱发收缩的阈去极化和收缩幅度。然而，5和10 mM咖啡因或10 mM普鲁卡因处理可提高力学阈值并抑制力学反应。普鲁卡因和咖啡因加速了无钙（EGTA）溶液储存部位Ca++的耗竭，并抑制了化学刺激诱导的力学反应。咖啡因和普鲁卡因抑制了去甲肾上腺素或前列腺素F2α引起的离子电导增加和去极化。咖啡因还抑制了上述药物诱导的力学反应。普鲁卡因抑制去甲肾上腺素诱导的收缩，但加速前列腺素F2α诱导的收缩。根据上述结果，得出结论：咖啡因和普鲁卡因不仅作用于细胞内的钙储存部位，还作用于表面膜。这些药物的作用彼此不具有竞争性，因此表明假定为主要钙储存部位的内膜结构特性与横纹肌不完全相同。
