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钾离子抑制状态下大鼠比目鱼肌的兴奋诱导力恢复

Excitation-induced force recovery in potassium-inhibited rat soleus muscle.

作者信息

Nielsen O B, Hilsted L, Clausen T

机构信息

Department of Physiology, University of Aarhus, DK-8000 Arhus C, Denmark.

出版信息

J Physiol. 1998 Nov 1;512 ( Pt 3)(Pt 3):819-29. doi: 10.1111/j.1469-7793.1998.819bd.x.

DOI:10.1111/j.1469-7793.1998.819bd.x
PMID:9769424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2231245/
Abstract
  1. Excitation markedly stimulates the Na+-K+ pump in skeletal muscle. The effect of this stimulation on contractility was examined in rat soleus muscles exposed to high extracellular K+ concentration ([K+]o). 2. At a [K+]o of 10 mM, tetanic force declined to 58 % of the force in standard buffer with 5.9 mM K+. Subsequent direct stimulation of the muscle at 1 min intervals with 30 Hz pulse trains of 2 s duration induced a 97 % recovery of force within 14 min. Force recovery could also be elicited by stimulation via the nerve. In muscles exposed to 12.5 mM K+, 30 Hz pulse trains of 2 s duration at 1 min intervals induced a recovery of force from 16 +/- 2 to 62 +/- 4% of the initial control force at a [K+]o of 5.9 mM. 3. The recovery of force was associated with a decrease in intracellular Na+ and was blocked by ouabain. This indicates that the force recovery was secondary to activation of the Na+-K+ pump. 4. Excitation stimulates the release of calcitonin gene-related peptide (CGRP) from nerves in the muscle. Since CGRP stimulates the Na+-K+ pump, this may contribute to the excitation-induced force recovery. Indeed, reducing CGRP content by capsaicin pre-treatment or prior denervation prevented both the excitation-induced force recovery and the drop in intracellular Na+. 5. The data suggest that activation of the Na+-K+ pump in contracting muscles counterbalances the depressing effect of reductions in the chemical gradients for Na+ and K+ on excitability.
摘要
  1. 兴奋可显著刺激骨骼肌中的钠钾泵。在暴露于高细胞外钾浓度([K⁺]o)的大鼠比目鱼肌中,研究了这种刺激对收缩性的影响。2. 在[K⁺]o为10 mM时,强直收缩力降至含5.9 mM K⁺的标准缓冲液中力的58%。随后以30 Hz、持续2 s的脉冲串每隔1分钟直接刺激肌肉,在14分钟内可使力恢复97%。通过神经刺激也可引起力的恢复。在暴露于12.5 mM K⁺的肌肉中,以30 Hz、持续2 s的脉冲串每隔1分钟刺激,可使力从初始对照力([K⁺]o为5.9 mM时)的16±2%恢复至62±4%。3. 力的恢复与细胞内钠的减少有关,并被哇巴因阻断。这表明力的恢复是钠钾泵激活的继发效应。4. 兴奋可刺激肌肉中神经释放降钙素基因相关肽(CGRP)。由于CGRP可刺激钠钾泵,这可能有助于兴奋诱导的力恢复。实际上,通过辣椒素预处理或预先去神经减少CGRP含量可防止兴奋诱导的力恢复以及细胞内钠的下降。5. 数据表明,收缩肌肉中钠钾泵的激活可抵消钠和钾化学梯度降低对兴奋性的抑制作用。

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