McKenna Michael J, Gissel Hanne, Clausen Torben
Department of Physiology, University of Aarhus, DK-8000 Arhus C., Denmark.
J Physiol. 2003 Mar 1;547(Pt 2):567-80. doi: 10.1113/jphysiol.2003.034512. Epub 2003 Jan 17.
Exercise has been reported to increase the Na+-K+-ATPase (Na+-K+ pump) alpha2 isoform in the plasma membrane 1.2- to 1.9-fold, purportedly reflecting Na+-K+ pump translocation from an undefined intracellular pool. We examined whether Na+-K+ pump stimulation, elicited by muscle contraction or insulin, increases the plasma membrane Na+-K+ pump content ([3H]ouabain binding) in muscles from young rats. Stimulation of isolated soleus muscle for 10 s at 120 Hz caused a rapid rise in intracellular Na+ content, followed by an 18-fold increase in the Na+ re-extrusion rate (80 % of theoretical maximum). Muscles frozen immediately or 120 s after 10-120 s stimulation showed 10-22 % decrease in [3H]ouabain binding expressed per gram wet weight, but with no significant change expressed per gram dry weight. In soleus muscles from adult rats, [3H]ouabain binding was unaltered after 10 s stimulation at 120 Hz. Extensor digitorum longus (EDL) muscles stimulated for 10-60 s at 120 Hz showed no significant change in [3H]ouabain binding. Insulin (100 mU ml-1) decreased intracellular Na+ content by 27 % and increased 86Rb uptake by 23 % soleus muscles, but [3H]ouabain binding was unchanged. After stimulation for 30 s at 60 Hz soleus muscle showed a 30% decrease in intracellular Na+ content, demonstrating increased Na+-K+ pump activity, but [3H]ouabain binding measured 5 to 120 min after stimulation was unchanged. Stimulation of soleus or EDL muscles for 120-240 min at 1 Hz (continuously) or 10 Hz (intermittently) produced no change in [3H]ouabain binding per gram dry weight. In conclusion, the stimulating effects of electrical stimulation or insulin on active Na+, K+-transport in rat skeletal muscle could not be even partially accounted for by an acute increase in the content of functional Na+ -K+ pumps in the plasma membrane.
据报道，运动可使质膜中的钠钾ATP酶（钠钾泵）α2亚型增加1.2至1.9倍，据称这反映了钠钾泵从一个未明确的细胞内池转运而来。我们研究了由肌肉收缩或胰岛素引发的钠钾泵刺激是否会增加幼鼠肌肉中质膜钠钾泵的含量（[3H]哇巴因结合）。以120Hz刺激离体比目鱼肌10秒，导致细胞内钠含量迅速升高，随后钠再排出率增加18倍（达到理论最大值的80%）。在刺激10至120秒后立即或120秒时冷冻的肌肉，每克湿重的[3H]哇巴因结合量减少了10%至22%，但每克干重表示时无显著变化。在成年大鼠的比目鱼肌中，以120Hz刺激10秒后，[3H]哇巴因结合未改变。以120Hz刺激趾长伸肌（EDL）10至60秒，[3H]哇巴因结合无显著变化。胰岛素（100mU/ml）使比目鱼肌细胞内钠含量降低27%，86Rb摄取增加23%，但[3H]哇巴因结合未改变。以60Hz刺激比目鱼肌30秒后，细胞内钠含量降低30%，表明钠钾泵活性增加，但刺激后5至120分钟测量的[3H]哇巴因结合未改变。以1Hz（持续）或10Hz（间歇）刺激比目鱼肌或EDL肌肉120至240分钟，每克干重的[3H]哇巴因结合无变化。总之，电刺激或胰岛素对大鼠骨骼肌中活性钠、钾转运的刺激作用，不能通过质膜中功能性钠钾泵含量的急性增加来部分解释。
