A KATP channel deficiency affects resting tension, not contractile force, during fatigue in skeletal muscle
A KATP channel deficiency affects resting tension, not contractile force, during fatigue in skeletal muscle
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DOI：
10.1152/ajpcell.2000.279.5.c1351
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发表时间：
2000-11-01
影响因子：
5.5
通讯作者：
Renaud, JM
中科院分区：
文献类型：
--
作者：
Gong, B;Miki, T;Renaud, JM
本研究的目的是确定atp敏感的K+ (K- atp)通道缺乏如何影响2- 3岁和1岁小鼠的指长伸肌（EDL）和比目鱼肌的收缩和疲劳特性。通过破坏编码形成通道孔的蛋白质的Kir6.2基因，获得K-ATP通道缺陷小鼠。在2 ~ 3月龄时，K-ATP通道缺陷小鼠EDL和比目鱼肌的力-频率曲线、抽搐力和强直力与野生型小鼠无显著差异。K-ATP通道缺陷小鼠EDL和比目鱼肌的强直力和最大力发展率随年龄的增长下降幅度（24-40%）大于野生型小鼠肌肉（7-17%）。疲劳时，K-ATP通道缺乏对EDL肌和比目鱼肌强直性力的降低没有影响，但与野生型小鼠相比，它引起肌肉静息张力的显著增加。2 ~ 3龄小鼠疲劳后的强直性力恢复不受K-ATP通道缺乏的影响，而1龄小鼠K-ATP通道缺乏肌肉的强直性力恢复明显低于野生型小鼠。这表明疲劳时K-ATP通道的主要功能是减少静息张力的发展，而不是导致力的下降。这也表明K-ATP通道在保护老年小鼠肌肉功能中起重要作用。
The objective of this study was to determine how an ATP-sensitive K+ (K-ATP) channel deficiency affects the contractile and fatigue characteristics of extensor digitorum longus (EDL) and soleus muscle of 2- to 3-mo-old and 1-yr-old mice. K-ATP channel-deficient mice were obtained by disrupting the Kir6.2 gene that encodes for the protein forming the pore of the channel. At 2-3 mo of age, the force-frequency curve, the twitch, and the tetanic force of EDL and soleus muscle of K-ATP channel-deficient mice were not significantly different from those in wild-type mice. However, the tetanic force and maximum rate of force development decreased with aging to a greater extent in EDL and soleus muscle of K-ATP channel-deficient mice (24-40%) than in muscle of wild-type mice (7-17%). During fatigue, the K-ATP channel deficiency had no effect on the decrease in tetanic force in EDL and soleus muscle, whereas it caused a significantly greater increase in resting tension when compared with muscle of wild-type mice. The recovery of tetanic force after fatigue was not affected by the deficiency in 2- to 3-mo-old mice, whereas in 1-yr-old mice, force recovery was significantly less in muscle of K-ATP channel-deficient than wild-type mice. It is suggested that the major function of the K-ATP channel during fatigue is to reduce the development of a resting tension and not to contribute to the decrease in force. It is also suggested that the K-ATP channel plays an important role in protecting muscle function in older mice.