Effects of denervation on sodium, potassium and [3H]ouabain binding in muscles of normal and potassium‐depleted rats.

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Abstract
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 was assessed in denervation experiments with K-depleted rats. In K-depleted rats (age 4-12 wk) denervation led to a partial recovery of the K contents in soleus (46-77%), gastrocnemius (23%) and extensor digitorum longus (EDL) 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 EDL 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. Anesthesia for 3 h increased the total K content by 23%. The recovery of K induced by denervation, immobilization in plaster, tenotomy or anesthesia 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 EDL. In both soleus and EDL the number of [3H]ouabain binding sites 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. The changes in Na-K contents seen after denervation in K-depleted rats are the outcome of cessation of muscle activity. No support is given 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.