1. This study explores the role of active electrogenic Na(+)‐K+ transport in restoring contractility in isolated rat soleus muscles exposed to high extracellular potassium concentration ([K+]o). This was done using agents (catecholamines and insulin) known to stimulate the Na(+)‐K+ pump via different mechanisms. 2. When exposed to Krebs‐Ringer bicarbonate buffer containing 10 mM K+, the isometric twitch and tetanic force of intact muscles decreased by 40‐69%. The major part of this decline could be prevented by the addition of salbutamol (10(‐5) M). In the presence of 10 mM K+, force could be restored almost completely within 5‐10 min by the addition of salbutamol or adrenaline and partly by insulin. 3. In muscles exposed to 12.5 mM K+, force declined by 96%. Salbutamol (10(‐5) M), adrenaline (10(‐6) M) and insulin (100 mU ml‐1) produced 57‐71, 61‐71 and 38‐47% recovery of force within 10‐20 min, respectively. The effects of these supramaximal concentrations of salbutamol and insulin on force recovery were additive. Salbutamol and adrenaline produced significant recovery of contractility at concentrations down to 10(‐8) M (P < 0.005). 4. In soleus, the same agents stimulated 86Rb+ uptake and decreased intracellular Na+. These actions reflect stimulation of active Na(+)‐K+ transport and both showed a highly significant correlation to the recovery of twitch as well as tetanic force (r = 0.80‐0.88; P < 0.001). 5. The force recovery induced by salbutamol, adrenaline and insulin was suppressed by pre‐exposure to ouabain (10(‐5) M for 10 min or 10(‐3) M for 1 min) as well as by tetrodotoxin (10(‐6) M). 6. The observations support the conclusion that the inhibitory effect of high [K+]o on contractility in skeletal muscle can be counterbalanced by stimulation of active electrogenic Na(+)‐K+ transport, the ensuing increase in the clearance of extracellular K+ and in the transmembrane electrochemical gradient for Na+.