Buchanan Rasmus, Nielsen Ole Baekgaard, Clausen Torben
Department of Physiology, University of Aarhus, DK-8000 Aarhus C, Denmark.
J Physiol. 2002 Nov 15;545(1):229-40. doi: 10.1113/jphysiol.2002.023325.
In rat skeletal muscle, Na(+)-K(+) pump activity increases dramatically in response to excitation (up to 20-fold) or beta(2)-agonists (2-fold), leading to a reduction in intracellular Na(+). This study examines the time course of these effects and whether they are due to an increased affinity of the Na(+)-K(+) pump for intracellular Na(+). Isolated rat soleus muscles were incubated at 30 (o)C in Krebs-Ringer bicarbonate buffer. The effects of direct electrical stimulation on (86)Rb(+) uptake rate and intracellular Na(+) concentration (Na(+)) were characterized in the subsequent recovery phase. Na(+) was varied using monensin or buffers with low Na(+). In the Na(+) range 21-69 mM, both the beta(2)-agonist salbutamol and electrical stimulation produced a left shift of the curves relating (86)Rb(+) uptake rate to Na(+). In the first 10 s after 1 or 10 s pulse trains of 60 Hz, Na(+) showed no increase, but (86)Rb(+) uptake rate increased by 22 and 86 %, respectively. Muscles excited in Na(+)-free Li(+)-substituted buffer and subsequently allowed to rest in standard buffer also showed a significant increase in (86)Rb(+) uptake rate and decrease in Na(+). Na(+) loading induced by monensin or electroporation also stimulated (86)Rb(+) uptake rate but, contrary to excitation, increased Na(+). The increase in the rate of (86)Rb(+) uptake elicited by electrical stimulation was abolished by ouabain, but not by bumetanide. The results indicate that excitation (like salbutamol) induces a rapid increase in the affinity of the Na(+)-K(+) pump for intracellular Na(+). This leads to a Na(+)-K(+) pump activation that does not require Na(+) influx, but possibly the generation of action potentials. This improves restoration of the Na(+)-K(+) homeostasis during work and optimizes excitability and contractile performance of the working muscle.
在大鼠骨骼肌中，钠钾泵活性会因兴奋（高达20倍）或β₂ - 肾上腺素能激动剂（2倍）而显著增加，导致细胞内钠离子减少。本研究考察了这些效应的时间进程以及它们是否归因于钠钾泵对细胞内钠离子亲和力的增加。将分离的大鼠比目鱼肌在30℃的 Krebs - Ringer 碳酸氢盐缓冲液中孵育。在随后的恢复阶段，表征了直接电刺激对⁸⁶Rb⁺摄取率和细胞内钠离子浓度（[Na⁺]i）的影响。使用莫能菌素或低钠缓冲液改变[Na⁺]i。在21 - 69 mM的[Na⁺]i范围内，β₂ - 肾上腺素能激动剂沙丁胺醇和电刺激均使⁸⁶Rb⁺摄取率与[Na⁺]i的关系曲线左移。在60 Hz的1或10 s脉冲串后的最初10 s内，[Na⁺]i未增加，但⁸⁶Rb⁺摄取率分别增加了22%和86%。在无钠锂替代缓冲液中兴奋并随后在标准缓冲液中静置的肌肉，其⁸⁶Rb⁺摄取率也显著增加，[Na⁺]i降低。莫能菌素或电穿孔诱导的钠离子加载也刺激了⁸⁶Rb⁺摄取率，但与兴奋相反，增加了[Na⁺]i。哇巴因可消除电刺激引起的⁸⁶Rb⁺摄取率增加，而布美他尼则不能。结果表明，兴奋（如沙丁胺醇）会诱导钠钾泵对细胞内钠离子的亲和力迅速增加。这导致钠钾泵激活，该激活不需要钠离子内流，但可能需要动作电位的产生。这改善了工作期间钠钾稳态的恢复，并优化了工作肌肉的兴奋性和收缩性能。
