The role of K+ channels in the force recovery elicited by Na+-K+ pump stimulation in Ba2+-paralysed rat skeletal muscle

1. The present experiments were performed to assess the role of K+ channels in hormonal stimulation of the Na+-K+ pump and to determine the contributi on of Na+-K+ pumps to the recovery of excitability and contractility in dep olarized skeletal muscle. 2. In soleus muscle, Ba2+ (0.02 and 1 mM) was found to inhibit K-42(+) effl ux and K-42(+) influx. Both in the absence and the presence of Ba2+ (1 mM), salbutamol and calcitonin gene-related peptide (CC;RP) induced a marked de crease in intracellular Na+ and stimulation of K-42(+) uptake. 3. In soleus muscles Ba2+ (0.1 and 1.0 mM) decreased twitch and tetanic for ce. Subsequent stimulation of the Na+-K+ pumps by salbutamol, CGRP or repea ted electrical stimulation produced a highly significant restoration of for ce development, which was suppressed by ouabain, but not by glibenclamide. Also, in extensor digitorum longus muscles Ba2+ (0.1 mM) produced a conside rable force decline, which a as partly restored by salbutamol and CGRP. 4. The area of compound action potentials (M-waves) elicited by indirect st imulation was decreased by Ba2+ (0.1 mM). This was associated with a concom itant decrease in tetanic force and depolarization. Salbutamol, CGRP or rep eated electrical stimulation all elicited marked recovery of M-wave area, f orce and membrane potential. All recordings showed close correlations betwe en these three parameters. 5. The data add further support to the concept that due to its electrogenic nature and large transport capacity, the Na+-K+ pump is a rapid and effici ent mechanism for the maintenance of excitability in skeletal muscle, actin g independently of Ba2+- or ATP-sensitive K+ channel function.