Active Na—K transport and the rate of ouabain binding. The effect of insulin and other stimuli on skeletal muscle and adipocytes

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Abstract
The effect of stimulation or inhibition of active Na-K transport on [3H]ouabain binding was investigated in isolated soleus muscles and adipocytes. In rat soleus muscle, the ouabain-sensitive component of 42K influx was stimulated by insulin (100 mu[milliunits]ml), adrenaline [epinephrine] (6 .times. 10-6 M), and by pre-incubation with veratrine (10-5 M) or in a K-free buffer. In all of these instances, the rate of ouabain binding was increased by 41-113%. Conversely, pre-treatment with tetracaine (0.2 mM) decreased the 42K-influx and diminished the rate of [3H]ouabain binding by 36%. Neither insulin, adrenaline or tetracaine produced any detectable change in the total number of ouabain-binding sites (as measured under equilibrium conditions) in rat soleus muscle. In mouse and guinea-pig soleus muscle and in fat cells isolated from rats, insulin also increased the rate of [3H]ouabain binding without producing any significant change in the total number of ouabain-binding sites. Both in soleus muscle and the epididymal fat pad of the rat, there was a linear correlation between 42K influx and the initial rate of [3H]ouabain binding. The rate of ouabain binding is determined significantly by the rate of active Na-K transport, but within the time intervals studied (4-6 h) stimulation or inhibition of the Na pump does not lead to any appreciable change in the total number of Na pumps. It seems unlikely that the stimulation of active Na-K transport by insulin or adrenaline is due to unmasking or de novo synthesis of Na pumps.

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