Sodium azide stimulated potassium efflux from striated muscles.

Abstract

Sodium azide (NaN3) in concentrations as low as 0.25 mM was capable of altering potassium fluxes in frog sartorius muscle fibers. Influx of potassium was maximally reduced in the presence of 2.0 mM NaN3 to between 32 and 39% of control. All concentrations of azide tested increased potassium efflux, but above 2.0 mM NaN3 the rate constant for potassium (K-42) efflux increased continuously. After the addition of 3.0 mM NaN3 to the normal Ringer's solution the rate constant for potassium efflux increased from 267% to 358% over a 2 h period. The stimulation of potassium efflux by sodium azide was always greater than the reduction of potassium influx. Net intracellular sodium was unaltered by axide concentrations below 2.0 mM, but markedly increased in the presence of higher azide concentrations. Muscles were rapidly depolarized by sodium azide in both 2.5 mM KCl and 5.0 mM KCl Ringer's solution. At higher azide concentrations (>2.0 mM) the depolarization was constant and did not reflect the continuous loss of potassium ions. The loss of intracellular potassium which was not completely compensated by the gain of sodium was probably due to an increase in potassium permeability.