Effects of pH,potential, chloride and furosemide on passive Na+ and K+ effluxes from human red blood cells |
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Authors: | A. Martin M. Zade-Oppen Norma C. Adragna Daniel C. Tosteson |
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Affiliation: | (1) Department of Physiology and Biophysics, Harvard Medical School, Boston, Massachusetts;(2) Department of Physiology and Medical Biophysics, Uppsala University, Uppsala, Sweden;(3) Present address: Department of Physiology and Medical Biophysics, BMC, Box 572, S-751 23 Uppsala, Sweden;(4) Present address: Department of Pharmacology and Toxicology, Wright State University, School of Medicine, 45435 Dayton, OH;(5) Present address: Office of the Dean, Harvard Medical School, 25 Shattuck St., 02115 Boston, MA |
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Abstract: | Summary Ouabain-resistant effluxes from pretreated cells containing K+/Na+=1.5 into K+ and Na+ free media were measured.Furosemide-sensitive cation effluxes from cells with nearly normal membrane potential and pH were lower in NO3– media than in Cl– media; they were reduced when pH was lowered in Cl– media. When the membrane potential was positive inside furosemide increased the effluxes of Na+ and K+ (7 experiments). With inside-positive membrane potential thefurosemideinsensitive effluxes were markedly increased, they decreased with decreasing pH at constant internal Cl– and also when internal Cl– was reduced at constant pH. The correlation between cation flux and the membrane potential was different for cells with high or low internal chloride concentrations. The data with chloride47mm showed a better fit with the single-barrier model than with the infinite number-of-barriers model. With low chloride no significant correlation between flux and membrane potential was found. The data are not compatible with pure independent diffusion of Na+ and K+ in the presence of ouabain and furosemide. |
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Keywords: | erythrocyte membrane furosemide ion transport Na– K cotransport ouabain |
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