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Experimental physiology1993; 78(5); 685-695; doi: 10.1113/expphysiol.1993.sp003716

Volume-sensitive KCl co-transport and taurine fluxes in horse red blood cells.

Abstract: Potassium (using 86Rb+ as a tracer), amino acid and taurine fluxes were measured in horse red blood cells (RBCs). No volume-sensitive component of alanine and glycine transport was observed, and although volume-sensitive taurine fluxes were observed in most animals, their absolute magnitudes were small. K+ fluxes, however, were shown to be particularly volume sensitive; they were stimulated by cell swelling and inhibited by cell shrinkage. Sizeable fluxes were present at normal cell volumes. The volume-sensitive K+ flux was Cl- dependent and was abolished by Cl- replacement with methylsulphate. The Cl(-)-dependent K+ fluxes in horse red blood cells were stimulated by lowering in external pH to 6.9 and by treatment with the sulphydryl-reacting agent, N-ethylmaleimide. They were inhibited by the potent K(+)-Cl- co-transport inhibitor, DIOA, ([(dihydroindenyl)oxy]alkanoic acid) but were insensitive to the Na(+)-K(+)-Cl- co-transport inhibitors, frusemide and bumetanide. A Cl- channel inhibitor, 5-nitro-2-(phenylpropyl-amino)-benzoate (NPPB), produced partial inhibition. These results suggest that regulatory volume decrease in horse red blood cells is achieved predominantly by volume-sensitive K+ efflux mediated via a K(+)-Cl- co-transport system with similar properties to those observed in the red blood cells of other species. The significance of these findings and their rheological consequences are discussed.
Publication Date: 1993-09-01 PubMed ID: 8240799DOI: 10.1113/expphysiol.1993.sp003716Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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The research article investigates potassium and taurine fluxes, especially the volume-sensitive ones, in horse red blood cells. The potassium flux was highlighted as particularly volume sensitive, being stimulated by cell swelling and constrained by cell shrinkage. The results suggest horse red blood cells regulate their size mainly by the volume-sensitive potassium efflux mediated through a potassium-chloride co-transport system.

Study Methodology

  • The researchers measured the potassium (using 86Rb+ as a tracer), amino acid, and taurine fluxes in horse red blood cells (RBCs).
  • They conducted this study across different cells with varying volumes, observing the effects of cell swelling and shrinkage.
  • They also examined the dependence of potassium flux on the presence of chloride ions by replacing chloride with methylsulphate.
  • The researchers used a mélange of interpretive processes such as the lowering of external pH to 6.9, and treatment with the sulphydryl-reacting agent, N-ethylmaleimide to understand the behaviour and functionality of these cells.

Key Findings

  • In contrary to any volume-sensitive component of alanine and glycine transport, only volume-sensitive taurine fluxes were noticed in the majority of horse RBCs, although the absolute magnitudes were small.
  • It was discovered that the K+ fluxes were particularly volume sensitive. These fluxes were stimulated by cell swelling and were found to be reduced by cell shrinkage.
  • The volume-sensitive potassium flux was chloride ion-dependent and was cancelled when chloride was replaced with methylsulphate.
  • The chloride-dependent potassium fluxes in horse red blood cells was found to be encouraged by the lowering in external pH to 6.9 and by treatment with the sulphydryl-reacting agent, N-ethylmaleimide.
  • DIOA, a potent K+-Cl- co-transport inhibitor, impeded these fluxes, while inhibitors to Na+-K+-Cl- co-transporters, such as frusemide and bumetanide, showed no particular impact. However, a chloride channel inhibitor, NPPB, resulted in a partial inhibition.

Implications

  • These findings suggest a regulatory volume decrease in horse red blood cells is achieved mainly by a volume-sensitive potassium efflux mediated via a potassium-chloride co-transport system.
  • Such behaviour is consistent with the red blood cells of other species, reaffirming the potency and utility of potassium-chloride co-transport mechanisms in various biological entities.
  • The discussions following the testing results proffered significant implications on understanding physiological processes and potentially devising therapeutic interventions for blood cell volume-related anomalies.

Cite This Article

APA
Gibson JS, Ellory JC, Culliford SJ, Fincham DA. (1993). Volume-sensitive KCl co-transport and taurine fluxes in horse red blood cells. Exp Physiol, 78(5), 685-695. https://doi.org/10.1113/expphysiol.1993.sp003716

Publication

ISSN: 0958-0670
NlmUniqueID: 9002940
Country: England
Language: English
Volume: 78
Issue: 5
Pages: 685-695

Researcher Affiliations

Gibson, J S
  • Department of Veterinary Medicine, University of Cambridge.
Ellory, J C
    Culliford, S J
      Fincham, D A

        MeSH Terms

        • Animals
        • Bumetanide / pharmacology
        • Carboxylic Acids / pharmacology
        • Carrier Proteins / analysis
        • Carrier Proteins / physiology
        • Erythrocyte Volume / physiology
        • Erythrocytes / chemistry
        • Erythrocytes / metabolism
        • Erythrocytes / physiology
        • Ethylmaleimide / pharmacology
        • Female
        • Furosemide / pharmacology
        • Horses / blood
        • Humans
        • Hydrogen-Ion Concentration
        • Indenes / pharmacology
        • Male
        • Potassium / metabolism
        • Symporters
        • Taurine / metabolism

        Grant Funding

        • Wellcome Trust

        Citations

        This article has been cited 6 times.
        1. Frlic O, Seliškar A, Domanjko Petrič A, Blagus R, Heigenhauser G, Vengust M. Pulmonary Circulation Transvascular Fluid Fluxes Do Not Change during General Anesthesia in Dogs. Front Physiol 2018;9:124.
          doi: 10.3389/fphys.2018.00124pubmed: 29515463google scholar: lookup
        2. Adragna NC, Di Fulvio M, Lauf PK. Regulation of K-Cl cotransport: from function to genes. J Membr Biol 2004 Oct 1;201(3):109-37.
          doi: 10.1007/s00232-004-0695-6pubmed: 15711773google scholar: lookup
        3. Muzyamba MC, Cossins AR, Gibson JS. Regulation of Na+-K+-2Cl- cotransport in turkey red cells: the role of oxygen tension and protein phosphorylation. J Physiol 1999 Jun 1;517 ( Pt 2)(Pt 2):421-9.
        4. Campbell EH, Gibson JS. Oxygen-dependent K+ fluxes in sheep red cells. J Physiol 1998 Feb 1;506 ( Pt 3)(Pt 3):679-88.
        5. Honess NA, Gibson JS, Cossins AR. The effects of oxygenation upon the Cl-dependent K flux pathway in equine red cells. Pflugers Arch 1996 Jun;432(2):270-7.
          doi: 10.1007/s004240050133pubmed: 8662303google scholar: lookup
        6. Gibson JS, Hall AC. Stimulation of KCl co-transport in equine erythrocytes by hydrostatic pressure: effects of kinase/phosphatase inhibition. Pflugers Arch 1995 Jan;429(3):446-8.
          doi: 10.1007/BF00374163pubmed: 7761269google scholar: lookup