Carrier-mediated beta-D-hydroxybutyrate transport in brush-border membrane (maternal-sided) vesicles prepared from trophoblast rat placenta was studied. The existence of a carrier-mediated transport system for beta-D-hydroxybutyrate in brush-border membrane vesicles was substantiated by the strong inhibitory effect of the protein modifier p-chloromercuriphenyl sulfonic acid and by the saturability of beta-D-hydroxybutyrate uptake as a function of beta-D-hydroxybutyrate concentration. beta-D-hydroxybutyrate uptake was stimulated by the presence of an inward-directed proton gradient but not by an inward-directed Na+ gradient. The mechanism for transport of beta-D-hydroxybutyrate seems to be a beta-D-hydroxybutyrate/H+ symport and not a beta-D-hydroxybutyrate/OH- antiport because beta-D-hydroxybutyrate transport was not sensitive to 4,4-diisothiocyano-2,2'-stilbenedisulfonic acid or furosemide. The Km, Vmax, and kd calculated by applying the iteration procedure to the data were 16 mM, 58 nmol.mg-1.10 s-1, and 0 nL.mg-1.s-1, respectively. The beta-D-hydroxybutyrate transport system might be shared by other monocarboxylic acids, and the carrier shows reversibility and exchange properties. There were no significant changes in the kinetic parameters of the beta-D-hydroxybutyrate transport system during the last 3 d of gestation. Nevertheless, there was a significant increase in the capacity of the beta-D-hydroxybutyrate transport system in brush-border membrane vesicles prepared from fasted pregnant rats, suggesting that the rise in maternal ketone body levels occurring as a consequence of maternal starvation is concurrent with the stimulation of the activity of the beta-D-hydroxybutyrate placental carrier to supply the fetus with ketone bodies.(ABSTRACT TRUNCATED AT 250 WORDS)