Excitation- and β2-agonist-induced activation of the Na+-K+ pump in rat soleus muscle
Excitation- and β2-agonist-induced activation of the Na+-K+ pump in rat soleus muscle
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DOI：
10.1113/jphysiol.2002.023325
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发表时间：
2002-11-15
影响因子：
5.5
通讯作者：
Clausen, T
中科院分区：
文献类型：
--
作者：
Buchanan, R;Nielsen, OB;Clausen, T
在大鼠骨骼肌中，Na+-K+泵活性响应于兴奋（高达20倍）或β（2）-激动剂（2倍）而显著增加，导致细胞内Na+减少。本研究探讨了这些影响的时间过程，以及它们是否是由于细胞内Na+的Na+-K+泵的亲和力增加。将分离的大鼠比目鱼肌在30 ℃下在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Rb-86（+）摄取速率和细胞内Na+浓度（[Na+]（i））的影响。[Na+]（i）使用莫能菌素或具有低Na+的缓冲液而变化。在[Na+]（i）21-69 mm范围内，β（2）-激动剂沙丁胺醇和电刺激均使Rb-86（+）摄取率与[Na+]（i）的关系曲线左移。在60 Hz的1或10 s脉冲串后的前10 s内，[Na+]（i）未显示增加，但Rb-86（+）摄取率分别增加22%和86%。在无Na+的Li+取代的缓冲液中兴奋并随后在标准缓冲液中休息的肌肉也显示Rb-86（+）摄取速率显著增加和[Na+]（i）降低。莫能菌素或电穿孔诱导的Na+负荷也刺激Rb-86（+）摄取速率，但与兴奋相反，增加[Na+]（i）。由电刺激引起的Rb-86（+）摄取率的增加被哇巴因消除，但布美他尼没有。结果表明，激发（如沙丁胺醇）诱导的Na+-K+泵的亲和力迅速增加，细胞内Na+。这导致Na+-K+泵激活，其不需要Na+流入，但可能产生动作电位。这改善了工作期间Na+-K+稳态的恢复，并优化了工作肌肉的兴奋性和收缩性能。
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 30degreesC in Krebs-Ringer bicarbonate buffer. The effects of direct electrical stimulation on Rb-86(+) uptake rate and intracellular Na+ concentration ([Na+](i)) were characterized in the subsequent recovery phase. [Na+](i) was varied using monensin or buffers with low Na+. In the [Na+](i) range 21-69 mm, both the beta(2)-agonist salbutamol and electrical stimulation produced a left shift of the curves relating Rb-86(+) uptake rate to [Na+](i). In the first 10 s after 1 or 10 s pulse trains of 60 Hz, [Na+](i) showed no increase, but Rb-86(+) 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 Rb-86(+) uptake rate and decrease in [Na+](i). Na+ loading induced by monensin or electroporation also stimulated Rb-86(+) uptake rate but, contrary to excitation, increased [Na+](i). The increase in the rate of Rb-86(+) 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.