Azide (0.2 to 5.0 mM) and chloretone (2.0 to 15.0 mM) reversibly inhibited 20 to 90 per cent of the resting respiration of frog sciatic nerves, and caused a loss of potassium and a gain of sodium in this tissue. The changes in ionic contents that developed after 5 or 10 hours were roughly correlated with the degree of respiratory depression, but the time courses of these changes were different with the two reagents. In azide these changes appeared to begin immediately, while in chloretone, at concentrations between 3.0 and 5.0 mM, the ionic shifts developed after a delay of several hours. Fifteen millimolar chloretone produced immediate changes in ionic contents several times greater than those produced by anoxia. The changes in ionic distribution produced in 5 hours by anoxia, 5.0 mM azide, or 5.0 mM chloretone were at least partially reversible; those produced by 15.0 mM chloretone were irreversible. With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway. Concentrations of azide or chloretone that depressed the resting rate of oxygen consumption more than 50 per cent produced a slow conduction block, while 15.0 mM chloretone blocked conduction within 15 minutes.

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