Respiration initiates Na+ efflux from Na+-preloaded cells of the halotolerant bacterium, Ba1. This efflux can take place against the concentration and electrochemical gradients. Since it is not inhibited by carbonylcyanide-p-trifluoromethoxyphenyl-hydrazone or N'N'-dicyclohexylcarbodiimide, it seems unlikely that either delta p (electrochemical potential difference of H+ across the membrane) generated by the primary proton pump or ATP play a role in the transduction of the energy supplied by electron transport. The electrogenic extrusion of Na+ causes passive counterflow of protons and/or simultaneous flux of permeant anions. In the absence of permeant anions the charge compensation attained by influx of protons is not complete. The membrane potential which persists in this case is inside negative and insensitive to uncoupler. The influx of protons builds up a delta pH of reversed sign (more acid inside), which is insensitive to uncoupler. The simultaneous efflux of Na+ and permeant anions diminishes the intracellular salt content and, as a corollary, causes volume contraction. Thus, the respiration-linked, uncoupler-insensitive Na+ pump may play a role in the regulation of the intracellular salt content.