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Chloride-Dependent Cation Transport in Human Erythrocytes

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Part of the book series: Contemporary Biomedicine ((CB,volume 10))

Abstract

When the sodium pump was identified 30 years ago in Glynn’s classical experiments on human red-cell Na and K fluxes (Glynn, 1956, 1957), the ouabain-insensitive monovalent cation fluxes were regarded as simply dissipative. It seemed that cell volume regulation could be explained by a two-component pump-leak model (Tosteson and Hoffman, 1960), but even then, the saturation kinetics displayed by the nonpump tracer K and Na influxes precluded a simple description as electrodiffusion. Since that time, it has become clear that ouabain-insensitive movements of Na and K occur via specific membrane transport systems, which show kinetic properties consistent with carriers or channels. A number of pathways for K transport are recognized: the Ca-activated (Gardos) channel, the NaKCl cotransport system, and the KCl cotransporter; for Na, NaKCl cotransport, Na-H and Na-Li exchanges, NaCO -3 anion exchange via capnophorin, and the Na-dependent amino-acid transporters asc and gly are significant contributors to transport (Ellory and Tucker, 1983). It is obvious that it is necessary to characterize these transport systems in order to understand the maintenance of intracellular ionic composition and, therefore, volume regulation in red cells (as a model system) and hence other cell types.

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Stewart, G.W., Ellory, J.C. (1989). Chloride-Dependent Cation Transport in Human Erythrocytes. In: Raess, B.U., Tunnicliff, G. (eds) The Red Cell Membrane. Contemporary Biomedicine, vol 10. Humana Press. https://doi.org/10.1007/978-1-4612-4500-1_13

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