Active transport of sodium and potassium in mammalian skeletal muscle and its modification by nerve and by cholinergic and adrenergic agents

1. Active transport of Na+ and K+ by Na-rich extensor digitorum and soleus muscles of rat was found to be increased considerably when muscles were innervated during enrichment with Na+ in K-free modified Krebs solution containing 160 m M-Na at 2° C and recovery in a similar fluid with 10 m M-K and 137 m M-Na at 37° C, bubbled with oxygen. 2. Addition of acetylcholine (2·0 μg/ml.) to recovery fluid containing denervated extensors increased active transport, whereas addition of eserine (50 μg/ml.), decamethonium (0·1 μg/ml.) and to a lesser extent tubocurarine (0·26 μg/ml.) inhibited active transport. Blocking of nerve conduction in innervated extensor inhibited K+ uptake more than Na+ excretion. 3. The membrane potential of Na-rich extensor muscles measured soon after re-immersion in recovery fluid was higher in denervated than in innervated muscles. In the latter it was close to the K-equilibrium potential (EK). It is suggested that denervation here makes the Na-pump electrogenic by decreasing K+ uptake either by decreased permeability or by inactivating a K-pump. Evidence is presented that the latter is more likely. 4. Addition of isoprenaline to Na-rich soleus muscles in recovery fluid increased active transport and reduced the membrane potential measured soon after re-immersion in recovery fluid. The Na-pump still remained electrogenic in the presence of isoprenaline. It was suggested that isoprenaline might also stimulate the Na-pump, perhaps through activation of lactic dehydrogenase.