提高胞外钾引起的蛙骨骼肌咖啡因挛缩增强

用蛙胫前肌小束为材料, 研究了提高胞外钾K+]O对咖啡因挛缩的作用.K+]O从2 mmol/L提高到10或25 mmol/L, 由3 mmol/L咖啡因引起的挛缩明显增强.以PKC/PC (PKC和PC分别为在高钾和正常钾条件下的咖啡因挛缩)表示的咖啡因挛缩增强, 依赖K+]O和高钾作用时间.随着10 mmol/L K+]O作用时间延长, 直至10 min, 增强逐渐增加.但是, 25 mmol/L K+]O作用1 min时增强达到最大, 然后下降到对照.PKC/PC变化时程不能用高钾引起的去极化解释, 而与由相似K+]O引起的胞浆自由钙变化时程相符.提示, 至少在蛙骨骼肌, 高钾引起的咖啡因挛缩增强主要是由胞浆自由钙升高引起的.

Potentiation of caffeine-induced contracture by raising extracellular potassium in frog skeletal muscle

The effect of raising extracellular potassium (K+]o) on caffeine contracture was investigated, using small bundles dissected from frog anterior tibialis muscle. Elevating K+]o from the control of 2 mmol/L to 10 or 25 mmol/L significantly potentiated the contracture induced by 3 mmol/L caffeine. The potentiation represented by PKC/PC, where PKC and PC are the peak tension of the caffeine contracture evoked in high and normal K+]o respectively, was dependent on K+]o and the duration of conditioning high K+ exposure. With 10 mmol/L K+]o, the potentiation was gradually increased by prolonging conditioning exposure up to 10 min. On the contrary, with 25 mmol/L K+]o the potentiation reached a maximum within only 1 min, and then subsided to the control. These different time courses of PKC/PC could not be accounted for by high K+ induced depolarization, but were in general consistence with the time courses of the change in myoplasmic free calcium induced by corresponding high K+]o. It is suggested that, at least in frog skeletal muscle, the high K+]o induced potentiation of caffeine contracture is mainly due to an increase of myoplasmic free calcium.