Effects of urea and oxygen tension on K flux in sickle cells

K influx and efflux (both ouabain- and bumetanide-resistant) in haemoglobin S-containing red cells (sickle cells) were markedly stimulated by urea (> 0.25 M). Stimulation was rapid and reversible. Volume-sensitive KCl cotransport in both HbA or HbS red cells is thought to be O2-dependent but we s...

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Veröffentlicht in:Pflügers Archiv 1998-04, Vol.435 (5), p.740-742
Hauptverfasser: Culliford, S J, Ellory, J C, Gibson, J S, Speake, P F
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Ellory, J C
Gibson, J S
Speake, P F
description K influx and efflux (both ouabain- and bumetanide-resistant) in haemoglobin S-containing red cells (sickle cells) were markedly stimulated by urea (> 0.25 M). Stimulation was rapid and reversible. Volume-sensitive KCl cotransport in both HbA or HbS red cells is thought to be O2-dependent but we show here that urea-stimulated K fluxes in sickle cells were largely insensitive to O2 tension. Urea-stimulated K fluxes were not inhibited by lowering the external Ca concentration (with EGTA) but were abolished by Cl-substitution (with MeSO4 or NO3) or pretreatment of cells with the protein phosphatase inhibitor, calyculin A (0.1 muM). Results are consistent with a stimulatory action of urea on the KCl cotransporter, independent of oxygen tension, mediated via the phosphorylation cascade which regulates the transporter. The importance of this effect to the physiology and pathology of sickle cells is discussed.
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Stimulation was rapid and reversible. Volume-sensitive KCl cotransport in both HbA or HbS red cells is thought to be O2-dependent but we show here that urea-stimulated K fluxes in sickle cells were largely insensitive to O2 tension. Urea-stimulated K fluxes were not inhibited by lowering the external Ca concentration (with EGTA) but were abolished by Cl-substitution (with MeSO4 or NO3) or pretreatment of cells with the protein phosphatase inhibitor, calyculin A (0.1 muM). Results are consistent with a stimulatory action of urea on the KCl cotransporter, independent of oxygen tension, mediated via the phosphorylation cascade which regulates the transporter. 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subjects Anemia, Sickle Cell - blood
Chlorides - metabolism
Erythrocytes - drug effects
Erythrocytes - metabolism
Hemoglobin, Sickle
Humans
In Vitro Techniques
Ion Transport - drug effects
Oxygen - blood
Potassium - blood
Proteins
Sickle cell anemia
Urea - metabolism
Urea - pharmacology
title Effects of urea and oxygen tension on K flux in sickle cells
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