Ito Y, Kuriyama H
J Physiol. 1974 Jan;236(1):143-57. doi: 10.1113/jphysiol.1974.sp010427.
Effects of thymol (0.02-2 mM) on the electrical and mechanical activities of the smooth muscle cells of the guinea-pig taenia coli were investigated with either micro-electrode or double sucrose gap methods.1. Thymol, in a concentration of more than 0.03 mM, reduced the amplitude and maximum rate of rise of the spikes without any change of the membrane potential. When the concentration was increased to 0.3 mM, thymol completely blocked the spontaneous and evoked spike activities. In a concentration of more than 0.1 mM, thymol reduced the membrane resistance in proportion to the concentration without any change of the membrane potential.2. Ionic mechanisms involved in the effects of thymol on the membrane resistance were investigated in various ionic environments. The results showed that in concentrations below 0.5 mM thymol might selectively increase the Cl-conductance of the membrane. Participations of Na and K ion in the effects of thymol on the membrane resistance could be eliminated. However, at more than 1 mM, thymol increased the membrane conductance non-selectively. Excess Ca in the external solution partly suppressed the action of thymol on the taenia coli.3. Potentiation of the twitch tension was not observed on treatment with any concentration of thymol.4. After pre-treatment with thymol (0.5 mM), isotonic K Krebs solution depolarized the membrane and reduced the membrane resistance as observed in the absence of thymol. However, thymol completely suppressed the K-induced contracture.5. Application of excess Ca and acetylcholine during the maintained contracture evoked by isotonic K Krebs solution induced further development of the contracture. However, on pre-treatment with thymol, neither excess Ca nor acetylcholine could evoke a mechanical response in isotonic K Krebs solution.6. The results obtained from the present experiments are discussed in relation to the roles of Ca on the smooth muscle cells.
采用微电极或双蔗糖间隙法研究了百里香酚(0.02 - 2 mM)对豚鼠结肠带平滑肌细胞电活动和机械活动的影响。1. 浓度高于0.03 mM的百里香酚可降低锋电位的幅度和最大上升速率,而膜电位无变化。当浓度增加到0.3 mM时,百里香酚完全阻断自发和诱发的锋电位活动。浓度高于0.1 mM时,百里香酚按浓度比例降低膜电阻,而膜电位无变化。2. 在不同离子环境下研究了百里香酚影响膜电阻的离子机制。结果表明,浓度低于0.5 mM时,百里香酚可能选择性增加膜的Cl - 电导。Na和K离子参与百里香酚对膜电阻的影响可被排除。然而,浓度超过1 mM时,百里香酚非选择性增加膜电导。细胞外溶液中过量的Ca部分抑制了百里香酚对结肠带的作用。3. 用任何浓度的百里香酚处理均未观察到收缩张力增强。4. 用百里香酚(0.5 mM)预处理后,等渗K Krebs溶液使膜去极化并降低膜电阻,这与未用百里香酚时观察到的情况相同。然而,百里香酚完全抑制了K诱导的挛缩。5. 在等渗K Krebs溶液诱发的持续挛缩过程中施加过量的Ca和乙酰胆碱会导致挛缩进一步发展。然而,用百里香酚预处理后,在等渗K Krebs溶液中,过量的Ca和乙酰胆碱均不能诱发机械反应。6. 结合Ca在平滑肌细胞中的作用对本实验结果进行了讨论。