Human placental brush-border membrane Na(+)-pantothenate cotransport.
Membrane transport pathways for transplacental transfer of the water-soluble vitamin pantothenate were investigated by assessing the possible presence of a Na(+)-pantothenate cotransport mechanism in the maternal facing membrane of human placental epithelial cells. The presence of Na(+)-pantothenate cotransport was determined from radiolabeled tracer flux measurements of pantothenate uptake using preparations of purified brush-border membrane vesicles. Compared with other cations the imposition of an inward Na+ gradient stimulated vesicle uptake of pantothenate to levels approximately 40-fold greater than those observed at equilibrium. The observed stimulation of pantothenate uptake was not the result of indirect electrostatic coupling to an inside positive Na+ diffusion potential. In the absence of Na+ and pantothenate concentration gradients an inside negative voltage difference induced a Na(+)-dependent net influx of pantothenate, suggesting the presence of an electrogenic Na(+)-pantothenate cotransport mechanism. The effect of biotin on the kinetics of Na(+)-dependent pantothenate uptake and the effect of pantothenate on the kinetics of Na(+)-dependent biotin uptake suggested that placental absorption of biotin and pantothenate from the maternal circulation occurs by a common Na+ cotransport mechanism in apical brush-border membrane.
Grassl
S M
SM
Department of Pharmacology, State University of New York Health Science Center, Syracuse 13210.
D001692:Biological Transport / Q000187:drug effects; D001710:Biotin / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D006801:Humans; D007700:Kinetics; D008871:Microvilli / Q000187:drug effects / Q000378:metabolism*; D010205:Pantothenic Acid / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D012964:Sodium / Q000378:metabolism*
D010205:Pantothenic Acid; D001710:Biotin; D012964:Sodium