Farley J M, Miles P R
J Pharmacol Exp Ther. 1977 Apr;201(1):199-205.
The effects of acetylcholine (ACh) and K+ on tension and membrane potential were studied in order to determine the role of electromechanical and pharmacomechanical coupling in ACh-induced contractions of dog trachealis muscle. Potassium causes sustained contractions of the muscle via membrane depolarization, which appears to be related in a linear manner to the log of the external K+ concentration. From the K+ experiments a curve relating membrane potential and tension was obtained. The resting membrane potential of the trachealis is -30 +/- 1 mV. At a dose of 10(-7) M ACh the membrane is depolarized to about -55 mV and then at 10(-6) M ACh there is more depolarization to about -40 mV. At higher doses of drug there is no further change in membrane potential. The relationship between the dose of ACh and tension is much different. Contraction begins at 10(-7) M ACh but does not saturate until a dose of 10(-3) M is reached. The data were interpreted by using the relationship between EM and tension from the K+ experiments and the ACh dose-response curves as follows. At 10(-7) M ACh only pharmacomechanical coupling is involved in the contraction. At higher drug doses both pharmaco- and electromechanical coupling are involved, but pharmacomechanical coupling appears to play a much greater role. The maximal contribution of electromechanical coupling is approximately 30% of the contraction and this occurs at 10(-6) M ACh.
为了确定电机械偶联和药机械偶联在乙酰胆碱（ACh）诱导的犬气管平滑肌收缩中的作用，研究了乙酰胆碱（ACh）和钾离子（K⁺）对张力和膜电位的影响。钾离子通过膜去极化引起肌肉持续收缩，这似乎与细胞外钾离子浓度的对数呈线性关系。从钾离子实验中得到了一条膜电位与张力的关系曲线。气管平滑肌的静息膜电位为-30±1mV。在10⁻⁷M ACh剂量下，膜去极化至约-55mV，然后在10⁻⁶M ACh时，进一步去极化至约-40mV。在更高剂量的药物作用下，膜电位不再发生变化。ACh剂量与张力之间的关系则大不相同。收缩从10⁻⁷M ACh开始，但直到达到10⁻³M剂量时才达到饱和。利用钾离子实验中膜电位与张力的关系以及ACh剂量-反应曲线对数据进行了解释，结果如下：在10⁻⁷M ACh时，收缩仅涉及药机械偶联。在更高的药物剂量下，药机械偶联和电机械偶联均参与其中，但药机械偶联似乎发挥了更大的作用。电机械偶联的最大贡献约为收缩的30%，这发生在10⁻⁶M ACh时。
