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Taurocholate - sodium co-transport by brush-border membrane vesicles isolated from rat ileum

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Lücke,  Heinrich
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Stange,  Gertraud
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Kinne,  Rolf
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Murer,  Heini
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Citation

Lücke, H., Stange, G., Kinne, R., & Murer, H. (1978). Taurocholate - sodium co-transport by brush-border membrane vesicles isolated from rat ileum. Biochemical Journal, 174(3), 951-958. doi:10.1042/bj1740951.


Cite as: http://hdl.handle.net/21.11116/0000-0008-451B-D
Abstract
Uptake of taurocholate into brush-border membrane vesicles isolated from rat small intestine by a Ca2+ -precipitation method was investigated by using a rapid-filtration technique. Uptake of taurocholate by ileal brush-border membranes consisted of three phenomena: binding to the outside of the vesicles, transfer across the vesicle membrane and binding to the intravesicular compartment. The transport of taurocholate across the brush-border membranes was stimulated in the presence of Na+ compared with the presence of K+; stimulation was about 11-fold in the presence of a NaCl gradient (Nao>Nai), where the subscripts refer to `outside' and `inside' respectively, and 4-fold under equilibrium conditions for Na+ (Nao=Nai). In the presence of a Na+ gradient a typical `overshoot' phenomenon was observed. Membranes preloaded with unlabelled taurocholate showed an accelerated entry of labelled taurocholate (tracer exchange) in the presence of Na+ compared with the presence of K+. The stimulation by Na+ was observed only in membrane preparations from the ileum. Addition of monactin, an ionophore for univalent cations, decreased the Na+-gradient-driven taurocholate uptake. The Na+-dependent taurocholate transport showed saturation kinetics and the phenomenon of counterflow and was inhibited by glycocholate. Other cations such as Li+, Rb+ and Cs+ could not replace Na+ in its stimulatory action. When the electrical potential difference across the vesicle membrane was altered by establishing different diffusion potentials (anion replacement; K+ gradient±valinomycin) a more-negative potential inside stimulated Na+-dependent taurocholate transport. These data demonstrate the presence of a rheogenic (potential sensitive) Na+–taurocholate co-transport system in ileal brush-border membranes and support the hypothesis that the reabsorption of bile acids in the ileum is a secondary active uptake.