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1. Ethacrynic acid (2 mM) increased the sodium efflux from freshly dissected frog sartorius muscles. This increase was not observed in muscles previously treated with strophanthidin.

2. In strophanthidin-treated muscles, the addition of ethacrynic acid (2 mM) caused a reduction of sodium efflux. The value of efflux reached in these muscles is similar to that observed in muscles immersed in sodium-free solutions containing strophanthidin.

3. Ethacrynic acid reduced sodium influx into strophanthidin-treated muscles. Potassium influx was not affected by this substance. These findings suggest that the inhibitor blocks an exchange of sodium for sodium.

4. The increase in sodium efflux caused by ethacrynic acid did not result from depolarization nor from an increase in [Na]_i.

5. Ethacrynic acid caused only a reduction of sodium efflux in muscles previously loaded with sodium by prolonged immersion in potassium-free solutions at low temperatures.

6. A derivative of ethacrynic acid that lacks the ability to combine with sulphydryl (SH) groups did not reduce sodium efflux from muscles treated with strophanthidin.

7. Para-chloromercuribenzoic acid (PCMB) reduced sodium efflux from control and strophanthidin-treated muscles. This reduction seems to be restricted to the sodium dependent component of the efflux.

8. The inhibition of the sodium-dependent component of sodium efflux caused by ethacrynic acid and PCMB appears to have a similar mechanism, namely, the combination with SH groups.