Szücs G, Fuxreiter M, Sirkó E, Szállási A
Acta Physiol Hung. 1983;62(1):61-73.
The effects of physostigmine on the electrophysiological properties of the surface membrane and on the different steps of excitation-contraction coupling were studied on the skeletal muscle of the frog (Rana esculenta). On analysing the phase plane trajectories of electrically evoked action potentials it was found that, similarly to the previously described pH dependence of the depolarizing effect of the alkaloid [14], the physostigmine-induced inhibition of the voltage-dependent sodium and potassium conductances responsible for the generation of the spike was increased in correlation with the decrease of external hydrogen ion concentration (pH 6.4, 7.0 and 8.4). When performing examinations on cut muscle fibres using the single vaseline gap voltage clamp technique [9], physostigmine did not exert any characteristic effect on the strength-duration curve of the contraction threshold determined by short depolarizing pulses even at higher concentrations (2 and 10 mmol/l; pH 7.0). In some cases the value of the rheobase was shifted to a variable extent towards more negative membrane potentials. On using the metallochromic indicator dye antipyrylazo III it was found that the application of 2 mmol/l physostigmine (pH 7.0) decreased the amount of calcium released during the depolarizing pulses. To reach the contraction threshold, a smaller increase in calcium concentration was necessary in the presence of the alkaloid. The relaxing phase of contractions elicited by depolarizing pulses was slowed down due to 2 mmol/l (pH 7.0) physostigmine treatment although the rate of the falling phase of the calcium transients increased simultaneously. The decrease in external hydrogen ion concentration facilitated the development of modifications in the shape of the contractions. The conclusion was drawn that the effects of physostigmine exhibit pH dependence. The alkaloid decreases calcium release from the sarcoplasmic reticulum and increases the calcium sensitivity of the contractile proteins.
在食用蛙（Rana esculenta）的骨骼肌上研究了毒扁豆碱对表面膜电生理特性以及兴奋 - 收缩偶联不同步骤的影响。在分析电诱发动作电位的相平面轨迹时发现，与先前描述的生物碱去极化作用的pH依赖性类似[14]，毒扁豆碱诱导的对负责产生峰电位的电压依赖性钠和钾电导的抑制作用随着外部氢离子浓度（pH 6.4、7.0和8.4）的降低而增加。当使用单凡士林间隙电压钳技术[9]对切断的肌纤维进行检查时，即使在较高浓度（2和10 mmol/L；pH 7.0）下，毒扁豆碱对由短去极化脉冲确定的收缩阈值的强度 - 持续时间曲线也没有产生任何特征性影响。在某些情况下，基强度值在不同程度上向更负的膜电位偏移。使用金属显色指示剂染料安替比拉佐III时发现，施加2 mmol/L毒扁豆碱（pH 7.0）会减少去极化脉冲期间释放的钙量。在存在生物碱的情况下，达到收缩阈值所需的钙浓度增加较小。尽管钙瞬变下降阶段的速率同时增加，但2 mmol/L（pH 7.0）毒扁豆碱处理使去极化脉冲引起的收缩的舒张期减慢。外部氢离子浓度的降低促进了收缩形状改变的发展。得出的结论是，毒扁豆碱的作用表现出pH依赖性。该生物碱减少了肌浆网中钙的释放，并增加了收缩蛋白对钙的敏感性。
