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通过提高蛙骨骼肌细胞外钾离子浓度增强咖啡因诱导的挛缩

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

作者信息

Chen K Y, Zhu P H

机构信息

Unit of Cell Signal Transduction, Shanghai Institute of Physiology, Chinese Academy of Sciences, Shanghai 200031.

出版信息

Sheng Li Xue Bao. 1999 Apr;51(2):153-60.

PMID:11499009
Abstract

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.

摘要

利用从青蛙胫前肌分离出的小肌束,研究了提高细胞外钾离子浓度([K⁺]o)对咖啡因挛缩的影响。将[K⁺]o从2 mmol/L的对照水平提高到10或25 mmol/L,可显著增强由3 mmol/L咖啡因诱导的挛缩。用PKC/PC表示增强作用,其中PKC和PC分别是在高[K⁺]o和正常[K⁺]o条件下诱发的咖啡因挛缩的峰值张力,其依赖于[K⁺]o和高钾预处理的持续时间。在[K⁺]o为10 mmol/L时,通过将预处理时间延长至10分钟,增强作用逐渐增加。相反,在[K⁺]o为25 mmol/L时,增强作用仅在1分钟内达到最大值,然后降至对照水平。PKC/PC的这些不同时间进程不能用高钾诱导的去极化来解释,但总体上与相应高[K⁺]o诱导的肌浆游离钙变化的时间进程一致。提示至少在青蛙骨骼肌中,高[K⁺]o诱导的咖啡因挛缩增强主要是由于肌浆游离钙增加。

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