Clausen T, Kjeldsen K, Nørgaard A
J Physiol. 1983 Dec;345:123-34. doi: 10.1113/jphysiol.1983.sp014969.
K depletion leads to a selective loss of K from skeletal muscles, which is associated with a decrease in the number of [3H]ouabain binding sites. The significance of the nerve supply for these changes has been assessed in denervation experiments with K-depleted rats. In K-depleted rats (age 4-12 weeks) denervation led to a partial recovery of the K contents in soleus (46-77%), gastrocnemius (23%) and extensor digitorum longus (e.d.l.) muscles (19%) within 24 h. These effects were not prevented by beta-adrenoceptor blockade or mimicked by alpha-adrenoceptor blockade. In K-depleted rats the number of [3H]ouabain binding sites was not increased following denervation. In K-depleted rats 24 h of plaster immobilization of the entire hind limb caused 51% recovery of the total K content in soleus, whereas gastrocnemius and e.d.l. showed 49 and 16% recovery, respectively. Tenotomy for 3 h caused a rise in total K content of 33% in soleus muscles from K-depleted rats. Anaesthesia for 3 h increased the total K content by 23%. The recovery of K induced by denervation, immobilization in plaster, tenotomy or anaesthesia was associated with an equivalent decrease in Na content. Denervation performed before K depletion reduced the loss of K from soleus, but not from gastrocnemius and e.d.l. In both soleus and e.d.l. the number of [3H]ouabain binding sites, however, decreased to the same level as in the contralateral innervated muscles. Denervation reduced, but did not prevent, the increase in the number of [3H]ouabain binding sites seen after re-administration of K to K-depleted rats. It is concluded that the changes in Na-K contents seen after denervation in K-depleted rats are the outcome of cessation of muscle activity. The results give no support to the idea that the effects of K depletion on the K content and the number of [3H]ouabain binding sites in skeletal muscle are mediated by the peripheral nerves.
钾缺乏导致骨骼肌中钾的选择性丢失，这与[3H]哇巴因结合位点数量的减少有关。在对缺钾大鼠进行的去神经实验中，已评估了神经供应对这些变化的影响。在缺钾大鼠（4至12周龄）中，去神经导致比目鱼肌（46 - 77%）、腓肠肌（23%）和趾长伸肌（e.d.l.）肌肉中的钾含量在24小时内部分恢复。β-肾上腺素能受体阻断并不能阻止这些作用，α-肾上腺素能受体阻断也不能模拟这些作用。在缺钾大鼠中，去神经后[3H]哇巴因结合位点的数量并未增加。在缺钾大鼠中，对整个后肢进行24小时的石膏固定导致比目鱼肌中总钾含量恢复51%，而腓肠肌和趾长伸肌分别恢复49%和16%。对缺钾大鼠的比目鱼肌进行3小时的肌腱切断术导致总钾含量升高33%。麻醉3小时使总钾含量增加23%。去神经、石膏固定、肌腱切断术或麻醉所诱导的钾恢复与钠含量的相应减少有关。在钾缺乏之前进行去神经可减少比目鱼肌中钾的丢失，但不能减少腓肠肌和趾长伸肌中钾的丢失。然而，在比目鱼肌和趾长伸肌中，[3H]哇巴因结合位点的数量均降至与对侧受神经支配肌肉相同的水平。去神经减少了，但并未阻止，在给缺钾大鼠重新补充钾后所观察到的[3H]哇巴因结合位点数量的增加。得出的结论是，缺钾大鼠去神经后钠钾含量的变化是肌肉活动停止的结果。这些结果不支持钾缺乏对骨骼肌中钾含量和[3H]哇巴因结合位点数量的影响是由外周神经介导的这一观点。
