Choline inhibits the uptake of [ 14C]tetraethylammonium (TEA) by mouse kidney cortex slices incubated in Krebs-Ringer bicarbonate buffer (37°, pH 7.4)), aerated with O 2-CO 2 95:5 v/v%. Inhibition seemed to be of a competitive type. Stimulation of unidirectional [ 14C]TEA exit occurred when choline was added to the wash-out medium, and approached 'a maximum value with increasing choline concentrations. Enhancement of TEA exit by choline could be demonstrated in the presence of high external K + concentrations suggesting that it was not secondary to unspecific changes in the membrane potential. Initial [ 14C]TEA uptake was increased in slices preloaded with choline. This argues against the possibility that choline stimulates exit by displacing [ 14C]TEA from intracellular binding sites. Preloading the tissue with choline did not reduce relative [ 14C]TEA exit which indicates that stimulation of initial TEA uptake after choline preloading is due to an increase of TEA influx rather than to an inhibition of TEA efflux. The results suggest that choline and TEA share a common transport mechanism. Transfer of TEA across the membrane in both directions depends on the transconcentration of choline. The stimulation phenomenon may be an example of accelerative exchange diffusion.