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KMID : 0357220020140020151
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Journal of Korean Society Physical Therapy
2002 Volume.14 No. 2 p.151 ~ p.162
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The Effects of ATP - sensitive K^(+) Channel on the Muscle Fatigue in Mouse Skeletal Muscle Cell
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Abstract
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Abstract
Excitation-contraction coupling in skeletal muscle is process by which depolarization of the muscle fiber membrane, elicited by a nerve action potential, triggers the release of Ca´` from the sarcoplasmic reticulum(SR). The resulting rise in intracellular Ca=´ concentration([Ca"li) activates the troponin complex, thereby initiating the contraction of the muscle. The question remains as to what factors are involved in the inhibition of SR Ca´-´ release in fatigued muscle.
The purpose of this study was determine whether ATP-sensitive K´(KATP) channels are activated and contribute to decrease in [Ca"]i during fatigue development in the mouse skeletal muscle. To elucidate a role of KATP in relation to ECC, I measured the modulation effects of KATP channel blocker(glibenclamide) and opencr(pinacidil) on [Ca2ji after fatiguing electrical field stimulation(FEFS). Intracellular Ca 21 signals were recorded by conforcal laser microscopy(LSM 410) and monitored using the fluorescent Ca-´-sensitive indicator Fluo-3 AM.
The results of this study were as followed:
1. The relative [Ca"Ji after FEFS in the pre-glibenclamide-treated group was higher than the control. And relative JCa=´]i alter FEFS in the pre-pinacidii-treated group was lower than the control.
2. The relative JCa´-´Ji after FEFS for 3 min in the control, pre-glibenclamide-treated group and prepinacidil-treated group showed a similar pattern; the gradually significant decrease in [Ca´-´]i. But, these decreasing pattern was most significant in the control.
These findings suggest a tight relationship between KAIP and [Ca2*Ji in ECC during fatigue. Therefore, I thought that activation of KA´rP channels may be one of mechanisms of the fatigue in skeletal muscle.
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KEYWORD
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