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

Abstract

1. The action of insulin on the transport and the distribution of Na and K has been studied in rat soleus muscles incubated at 30 degrees C in glucose‐free Krebs‐Ringer bicarbonate buffer. 2. Measurements of the uptake and the wash‐out of 22Na indicate that the muscles contain an intracellular pool of Na available for transport which is confined to the water space not available to sucrose. Ouabain (10(‐4)‐10(‐3)M) inhibited 22Na efflux by 69% (0‐287 micronmole/g tissue wet weight per minute) and 42K‐influx by 40% (0‐196 micronmole/g tissue wet weight per minute). When all extracellular Na was replaced by Li, both 22Na‐efflux adn 42K‐influx were inhibited to about the same extent and ouabain produced very little further inhibition. 2,4‐dinitrophenol decreased the ouabain‐resistant component of 22Na‐efflux by 39%. 3. Insulin (from 0‐1 to 100 mu./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 stimulates 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 X 10(‐3)M), phlorizin (0‐5 X 10(‐2)M) or by the substitution of Na, K, Mg or Ca. In the presence of 2,4‐dinitrophenol (0‐5 X 10(‐4)M) or at temperatures below 15 degrees C, the hormone produced no detectable change in 22Na‐efflux. 4. Insulin increased 42K‐influx from 0‐525 to 0‐664 mumole/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. 5. The continued exposure to insulin led to a new steady state, in which the intracellular Na pool was decreased from around 10 to around 5 mumole/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 around 35%. This effect was blocked by 2,4‐dinitrophenol but not be tetracaine. 6. It is concluded that insulin stimulates the active coupled transport of Na and K, possibly by increasing the relative Na‐affinity of the system mediating this process.