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      Acute Regulation of the Betaine/GABA Transporter BGT-1 Expressed in Xenopus Oocytes by Extracellular pH

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          Besides uptake of Na<sup>+</sup> and Cl<sup>–</sup>, mammalian cells counteract osmotic cell shrinkage also by Na<sup>+</sup>-coupled uptake of osmolytes, e.g., myo-inositol, taurine or betaine. The expression of the corresponding transporters is transcriptionally regulated by the ambient pH and osmolarity and is increased upon cell shrinkage, a process requiring hours. The present study has been performed to disclose rapid regulation by pH of osmolyte transport via BGT-1. Transport of GABA was investigated by using the two-electrode voltage-clamp technique with BGT-1 expressing Xenopus oocytes. GABA was used as a substrate, because of the low oocyte endogenous transport activity. Extracellular acidification to pH 5.5 reversibly decreased and extracellular alkalinization to pH 8.5 increased GABA-induced currents. Kinetic analysis revealed that extracellular alkalinization increases the affinity for Cl<sup>–</sup> as reflected by a decrease of the apparent K<sub>m</sub>-value for Cl<sup>–</sup> from >500 m M to 55.8 ± 4.7 m M upon an increase of the pH from 7.0 to 8.5. The apparent K<sub>m</sub>- values for Na<sup>+</sup> and GABA remained unaltered in the pH range from 6.0 to 8.5. Instead, alkalinization increased the maximal current induced by saturating Na<sup>+</sup> and GABA concentrations. The results are compatible with a model of interference of H<sup>+</sup> ions with Cl<sup>–</sup> binding and a pH-dependent reduction of V<sub>max</sub> for Na<sup>+</sup> and GABA.

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          Most cited references 5

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          The Diversity of Volume Regulatory Mechanisms

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            Swelling-activated organic osmolyte channels.

             K. Kirk Shung (1997)
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              Functional Characterization of the Betaine/γ-Aminobutyric Acid Transporter BGT-1 Expressed inXenopusOocytes


                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                02 November 2000
                : 23
                : 6
                : 356-359
                aDepartment of Physiology, University of Tübingen, Germany; bSechenov Institute of Comparative Physiology and Biochemistry, St. Petersburg, Russia; cInstitute for Cellular Signaling, University of Nijmegen, The Netherlands
                25983 Kidney Blood Press Res 2000;23:356–359
                © 2000 S. Karger AG, Basel

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                Figures: 3, References: 26, Pages: 4
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/25983
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