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- W2022331609 abstract "Abstract Recently we have reported evidence for Cl − /HCO 3 − exchange in A10 vascular smooth muscle cells (ATCC CRL 1476) by means of continuous intracellular pH measurements (Korbmacher, C., Helbig, H., Stahl, F. and Wiederholt, M. (1988) Pflugers Arch. 412, 29–36). In the present study we used 36 Cl − to further characterize Cl − /HCO 3 − exchange in confluent monolayers of A10 cells. Under the chosen experimental conditions, 36 Cl − uptake was inhibited by more than 90% in the presence of the stilbene derivatives SITS (1 mM) and DIDS (1 mM), known inhibitors of Cl − /HCO 3 − exchange. The IC 50 for DIDS was about 5 μM. Ethacrynic acid was also an effective inhibitor of 36 Cl − uptake with an IC 50 of about 20 μM. ‘Loop diuretics’ (furosemide, bumetanide) and ‘Cl − -channel blockers’ (DPC, A9C, NPPB) had only small effects on 36 Cl − uptake in concentrations in which they are thought to act specifically on Na + /K + /2Cl − cotransport or on chloride channels, respectively. DIDS-sensitive 36 Cl − uptake was a saturable function of the extracellular chloride concentration with an apparent K m for extracellular chloride of about 45 mM. 36 Cl − uptake was inhibited by the presence of extracellular HCO 3 − , Br − , I − , acetate − and NO 3 − . 36 Cl − uptake could be stimulated by bicarbonate-preloading of the cells. Intracellular alkalinization during the uptake period (induced by application of NH 4 + ) also stimulated 36 Cl − uptake. 36 Cl − efflux was greater in the presence than in the absence of extracellular chloride or bicarbonate. 36 Cl − efflux was diminished in the presence of 1 mM DIDS. In conclusion our data are compatible with a DIDS-sensitive Cl − /HCO 3 − exchange which is stimulated by intracellular alkalinization." @default.
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- W2022331609 date "1989-10-01" @default.
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- W2022331609 title "Characterization of Cl−/HCO3− exchange in A10 vascular smooth muscle cells using 36Cl−" @default.
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- W2022331609 doi "https://doi.org/10.1016/0005-2736(89)90105-3" @default.
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