Activation by N-ethylmaleimide of a latent K+-Cl- flux in human red blood cells
| Autor: | P. K. Lauf, N. C. Adragna, R. P. Garay |
|---|---|
| Rok vydání: | 1984 |
| Předmět: |
Erythrocytes
Physiology Stereochemistry Potassium Biological Transport Active chemistry.chemical_element Potassium Chloride Blood cell chemistry.chemical_compound Flux (metallurgy) Furosemide medicine Humans heterocyclic compounds Ouabain Bumetanide Sodium N-Ethylmaleimide Cell Biology Membrane transport Rubidium Molecular biology Kinetics Red blood cell medicine.anatomical_structure chemistry Ethylmaleimide Cotransporter |
| Zdroj: | American Journal of Physiology-Cell Physiology. 246:C385-C390 |
| ISSN: | 1522-1563 0363-6143 |
| DOI: | 10.1152/ajpcell.1984.246.5.c385 |
| Popis: | Twenty to fifty percent of the ouabain-insensitive Na+ and K+ fluxes in human red blood cells are mediated by Cl(-) -dependent coupled transport (cotransport). In this paper we report on the effect of the sulfhydryl group reagent N-ethylmaleimide (NEM) on Cl(-) -dependent ouabain-insensitive Na+ and K+ fluxes in human red blood cells. We found that NEM altered Na+ -K+ cotransport and activated a latent Cl(-) -dependent K+ transport mode normally apparently silent. This conclusion was based on the following observations. 1) At low concentrations (0.25 mM) NEM abolished the bumetanide-sensitive Na+ efflux and had no effect, even at a 10-fold higher concentration, on the bumetanide-sensitive K+ efflux. 2) At concentrations above 0.1 mM, NEM stimulated Cl(-) -dependent K+ efflux that was only partially inhibited by high concentrations of bumetanide or furosemide. In experiments using Rb+ as a K+ analogue, NEM activated Rb+ influx by stimulating the maximum velocity and lowering the apparent external cation affinity. The data suggest the presence of chemically reactive groups in human red blood cells for both Cl(-) -dependent K+ transport activated by NEM and Cl(-) -dependent coupled Na+-K+ movements. |
| Databáze: | OpenAIRE |
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