Taurine transport into six brain regions of equithesin-anesthetized rats was studied by the in situ brain perfusion technique. This technique gives both accurate measurements of cerebrovascular amino acid transport and allows complete control of the perfusate amino acid composition. Final wash procedure showed that taurine efflux occurred rapidly from endothelial cells. The taurine influx into endothelial cells was sodium and chloride dependent suggesting that the sodium and chloride gradients are the principal source of energy for taurine transport into endothelial cells. Taurine transport could be fitted by a model with saturable components. The kinetic constants in the parietal cortex were 1.4 x 10(-4) mumol/s/g for the apparent Vmax and 0.078 mM for the apparent Km. Competition experiments in the presence of sodium ions showed that [14C]taurine uptake was strongly inhibited by the structural analogs of taurine, hypotaurine and beta-alanine.