Effects of 17β-estradiol on tension responses and fatigue in the skeletal twitch muscle fibers of frog
Effects of 17β-estradiol on tension responses and fatigue in the skeletal twitch muscle fibers of frog
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DOI：
10.2170/jjphysiol.51.753
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发表时间：
2001-12-01
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影响因子：
--
通讯作者：
Hatae, J
中科院分区：
文献类型：
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作者：
Hatae, J
本文研究了活性雌激素17β-雌二醇(10(-5)M)对蛙骨骼肌单纤维或纤维束张力和疲劳反应的影响。给予17β-雌二醇每分钟场强刺激可引起破伤风张力的一过性增强。这种增强作用不受尼卡地平的影响，提示17β-雌二醇的作用将使兴奋-收缩(E-C)偶联超越T管去极化。疲劳是通过每秒重复的强直性刺激产生的，直到张力下降到最初水平的大约40%。然后，通过每分钟给纤维注射破伤风，纤维得以恢复。在正常林格液中，破伤风初始张力达到50%的时间为41.7 S，在17β-雌二醇存在下，达到50%张力的时间比对照组快。17α-雌二醇是一种立体异构体，它的存在不会使强直性张力每分钟增强一次，疲劳反应的下降速度几乎与对照组相同，提示蛙肌肉中存在特异的雌激素受体。在有或没有雌激素的疲劳肌肉中，对场刺激的张力是暂时的，不是持续的。当疲劳的肌肉在更频繁的刺激后每分钟再次进行场刺激时，17β-雌二醇的恢复率增加。在咖啡因存在的情况下，迅速将温度从20摄氏度降至5摄氏度会引发张力反应，即快速降温收缩(RCC)。只有在重复电刺激后，17β-雌二醇才能抑制RCC的最大张力和最大上升速率。这些结果提示，17β-雌二醇电刺激引起的收缩增强是通过激活E-C偶联过程引起的肌浆内游离钙离子浓度升高所致。17β-雌二醇易化对高频重复破伤风刺激的疲劳反应可能是由于胞浆内钙离子周转失衡增加所致。
The effects of 17beta-estradiol (10(-5) M), an active estrogen, on the tension and fatigue responses of single fiber or fiber bundle prepared from frog skeletal muscle were investigated. The administration of 17beta-estradiol caused a transient potentiation of tetanus tension by field stimulation at every minute. This potentiation was not affected by the presence of nicardipine, suggesting that the action of 17beta-estradiol would place the excitation-contraction (E-C) coupling beyond T-tubule depolarization. Fatigue was produced by repeated tetanic stimulation every second until tension declined to approximately 40% of the initial level. Fibers were then allowed to recover by having tetani given to them every minute. In the normal Ringer solution, the time to 50% of the initial tetanus tension was 41.7 s. With the presence of 17beta-estradiol, the time to 50% tension was faster than that of control. The presence of 17alpha-estradiol, a stereoisomer, caused no potentiation of tetanic tension to be stimulated every minute, and the rate of decline of fatigued response was almost the same as that of control, suggesting the existence of specific estrogen receptors in the frog muscle. In fatigued muscle with or without estrogen, the tension to field stimulation was transient and not sustained. When the fatigued muscle was again treated with field stimulation at every minute after the more-frequent stimulation, the recovery rate was increased in 17beta-estradiol. A prompt reduction in temperature to 5degreesC, from 20degreesC, in the presence of caffeine elicited the tension response, a rapid cooling contracture (RCC). The presence of 17beta-estradiol inhibited peak tension and maximum rate of rise of the RCC only after the repetitive electrical stimuli. These results suggest that the potentiation of contraction upon the electrical stimulation by 17beta-estradiol was induced by the increase of myoplasmic-free Ca2+ concentration via an activation of some E-C coupling process. The 17beta-estradiol-induced facilitation of fatigue response to repetitive tetanus stimuli with high frequency may be due to an increase in the imbalance of Ca2+ turnover in the cytoplasm.