Peiper U
J Cardiovasc Pharmacol. 1984;6 Suppl 2:S328-35. doi: 10.1097/00005344-198406002-00007.
Contraction kinetics of smooth-muscle preparations (rat portal vein, rat tracheal muscle) were studied by means of force-velocity relations obtained from after-loaded isotonic contractions or from the analysis of the isometric tension increase. Furthermore, the time constant of the tension recovery following an inhibiting length vibration reflected the contraction kinetics as well. Signals that induce changes in the calcium concentration or the area of overlap between actin and myosin cause changes mainly in the number of acting cross-bridges. Decrease in temperature, pH reduction, and a long-term stimulation induce slower contraction kinetics probably because of a lesser myosin light-chain kinase activity. The results obtained give further evidence for different mechanisms controlling extent and rate of smooth-muscle contraction.
通过后负荷等张收缩获得的力-速度关系或等长张力增加的分析,研究了平滑肌制剂(大鼠门静脉、大鼠气管平滑肌)的收缩动力学。此外,抑制性长度振动后张力恢复的时间常数也反映了收缩动力学。诱导钙浓度或肌动蛋白与肌球蛋白重叠面积变化的信号主要引起肌动蛋白横桥数量的变化。温度降低、pH值降低和长期刺激可能由于肌球蛋白轻链激酶活性降低而导致收缩动力学减慢。所获得的结果进一步证明了控制平滑肌收缩程度和速率的不同机制。