Sodium and Chloride Ion‐Dependent Transport of β‐Alanine Across the Blood‐Brain Barrier

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Abstract
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‐[3H]alanine transport indicated that the transporter for β‐alanine functions with Kt of 25.3 ± 2.5 µM and Jmax of 6.90 ± 0.48 nmol/30 min/mg of protein in the brain capillary endothelial cells. β‐[3H]Alanine uptake is mediated by an active transporter, because metabolic inhibitors (2,4‐dinitrophenol and NaN3) and low temperature reduced the uptake significantly. Furthermore, the uptake of β‐[3H]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‐[3H]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‐[3H]alanine, whereas α‐ and γ‐amino acids had little or no inhibitory effect. In ATP‐depleted cells, the uptake of β‐[3H]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.

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