Krivoĭ I I, Kravtsova V V, Altaeva E G, Kubasov I V, Prokof'ev A V, Drabkina T M, Nikol'skiĭ E E, Shenkman B S
Biofizika. 2008 Nov-Dec;53(6):1051-7.
After three days of hind limb unloading, the depolarization of muscle fibers from -71.0 +/- 0.5 mV to -66.8 +/- 0.7 mV as well as a decrease in muscle excitability and a trend to fatigue acceleration were observed. After hind limb unloading, the electrogenic contribution of the ouabain-sensitive alpha2 isoform of Na,K-ATPase, tested as depolarization due to the administration of 1 microM ouabain, decreased from 6.2 +/- 0.6 to 0.5 +/- 0.8 mV. The contribution of the ouabain-resistant alpha1 isoform, estimated as additional depolarization after the administration of 500 microM ouabain, decreased from 4.6 +/- 0.6 to 2.6 +/- 0.6 mV. After hind limb unloading, the fluorescence intensity of single muscle fibers loaded with Fluo-4-AM increased more than four times, indicating an increase in intracellular Ca2+ concentration. The effect was prevented by local delivery of nifedipine, which blocks L-type Ca2+ channels. These data suggest the existence of a selective mechanism of suppression of the alpha2-pump electrogenic contribution, which led to the depolarization of soleus muscle fibers after 3 days of hind limb unloading. The depolarization in turn may activate L-type Ca2+ channels, resulting in intracellular Ca2+ accumulation.
后肢去负荷三天后，观察到肌纤维的去极化从-71.0±0.5 mV变为-66.8±0.7 mV，同时肌肉兴奋性降低，且有疲劳加速的趋势。后肢去负荷后，用1 microM哇巴因给药后测试的钠钾ATP酶哇巴因敏感α2亚型的电生成贡献从6.2±0.6 mV降至0.5±0.8 mV。用500 microM哇巴因给药后估计的哇巴因抗性α1亚型的贡献从4.6±0.6 mV降至2.6±0.6 mV。后肢去负荷后，加载Fluo-4-AM的单根肌纤维的荧光强度增加了四倍多，表明细胞内Ca2+浓度增加。该效应被局部递送的硝苯地平所阻止，硝苯地平可阻断L型Ca2+通道。这些数据表明存在一种选择性机制来抑制α2泵的电生成贡献，这导致后肢去负荷三天后比目鱼肌纤维去极化。去极化进而可能激活L型Ca2+通道，导致细胞内Ca2+积累。
