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Sodium and Chloride Ion‐Dependent Transport of β‐Alanine Across the Blood‐Brain Barrier
Author(s) -
Komura Junko,
Tamai Ikumi,
Senmaru Mizuho,
Terasaki Tetsuya,
Sai Yoshimichi,
Tsuji Akira
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.67010330.x
Subject(s) - alanine , hypotaurine , chemistry , taurine , sodium , amino acid , blood–brain barrier , biochemistry , biology , endocrinology , organic chemistry , central nervous system
The characteristics of β‐alanine transport at the blood‐brain barrier were studied by using primary cultured bovine brain capillary endothelial cells. Kinetic analysis of the β‐[ 3 H]alanine transport indicated that the transporter for β‐alanine functions with K t of 25.3 ± 2.5 µ M and J max of 6.90 ± 0.48 nmol/30 min/mg of protein in the brain capillary endothelial cells. β‐[ 3 H]Alanine uptake is mediated by an active transporter, because metabolic inhibitors (2,4‐dinitrophenol and NaN 3 ) and low temperature reduced the uptake significantly. Furthermore, the uptake of β‐[ 3 H]alanine required Na + and Cl − in the external medium. Stoichiometric analysis of the transport demonstrated that two sodium ions and one chloride ion are associated with one β‐alanine molecule. The Na + and Cl − ‐dependent uptake of β‐[ 3 H]alanine was stimulated by a valinomycin‐induced inside‐negative K + ‐diffusion potential. β‐Amino acids (β‐alanine, taurine, and hypotaurine) inhibited strongly the uptake of β‐[ 3 H]alanine, whereas α‐ and γ‐amino acids had little or no inhibitory effect. In ATP‐depleted cells, the uptake of β‐[ 3 H]alanine was stimulated by preloading of β‐alanine or taurine but not l ‐leucine. These results show that β‐alanine is taken up by brain capillary endothelial cells, via the secondary active transport mechanism that is common to β‐amino acids.