The effect of insulin on the transport of sodium and potassium in rat soleus muscle.

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Abstract
The action of insulin on the transport and the distribution of Na and K was studied in rat soleus muscles incubated at 30.degree. C in glucose-free Krebs-Ringer bicarbonate buffer. Measurements of the uptake and the wash-out of 22Na indicated that the muscles contained an intracellular pool of Na available for transport which was confined to the water space not available to sucrose. Ouabain (10-4-10-3 M) inhibited 22Na efflux by 69% (0.287 .mu.mol/g tissue wet weight per minute) and 42K-influx by 40% (0.196 .mu.mol/g tissue wet weight per minute). When all extracellular Na was replaced by Li, both 22Na-efflux and 42K-influx were inhibited to about the same extent and ouabain produced very little further inhibition. 2,4-Dinitrophenol [DNP] decreased the ouabain-resistant component of 22Na-efflux by 39%. Insulin (0.1-100 mu[milliunit]/ml) increased the rate coefficient of 22Na-efflux by from 11 to 46% within 15 min. In the presence of ouabain (10-3 M), the same relative increase was obtained, indicating that the hormone stimulated the glycoside-sensitive and the glycoside-insensitive Na transport to a similar extent. The effect of insulin on 22Na-efflux was not abolished by tetracaine (0.5 .times. 10-3 M), phlorizin (0.5 .times. 10-2 M) or by the substitution of Na, K, Mg or Ca. In the presence of DNP (0.5 .times. 10-4 M) or at temperatures below 15.degree. C, the hormone produced no detectable change in 22Na-efflux. Insulin increased 42K-influx from 0.525 to 0.664 .mu.mol/g tissue wet weight per minute. This effect was entirely blocked by ouabain but not by tetracaine. Insulin produced a 14% transient decrease in 42K-efflux. The continued exposure to insulin led to a new steady state, in which the intracellular Na pool was decreased from .apprx. 10 to .apprx. 5 .mu.mol/g tissue wet weight and the K content increased by an equivalent amount. In the presence of ouabain or at low extracellular concentrations of K, insulin increased the rate of 22Na-influx by .apprx. 35%. This effect was blocked by DNP but not by tetracaine. Insulin stimulated the active coupled transport of Na and K, possibly by increasing the relative Na-affinity of the system mediating this process.

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