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Pflugers Archiv : European journal of physiology1995; 429(3); 446-448; doi: 10.1007/BF00374163

Stimulation of KCl co-transport in equine erythrocytes by hydrostatic pressure: effects of kinase/phosphatase inhibition.

Abstract: The effects of hydrostatic pressure on the KCl co-transporter of equine erythrocytes were studied to determine factors involved in its regulation. Pressure (0.1-40MPa) increased Cl-dependent K+ transport; in the presence of the putative kinase inhibitor N-ethylmaleimide (NEM) which stimulates the transporter, or the phosphatase inhibitor calyculin A, pressure had no significant effect. The sequential application of NEM and calyculin A clamped the transporter at about 30% of maximal flux compared to NEM alone; pressure also had no further effect. These results suggest that pressure acts on the phosphorylation status of the transporter or regulatory peptide, rather than on the ion flux per se. Since the activation of the KCl co-transporter by pressure occurs without an apparent change in cell volume these results have implications for any universal model for the regulation of KCl co-transport.
Publication Date: 1995-01-01 PubMed ID: 7761269DOI: 10.1007/BF00374163Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research article investigates the regulation of the potassium-chloride (KCl) co-transporter in horse red blood cells, specifically focusing on how hydrostatic pressure influences it.

Overview of the Research

  • The study mainly investigates the effects of hydrostatic pressure on the potassium-chloride (KCl) co-transporter within horse red blood cells (erythrocytes). The co-transporter is a protein that helps to manage the balance of potassium and chloride ions within the cell.
  • In this experiment, pressure levels ranging from 0.1MPa to 40MPa were applied to analyse the impacts on KCl co-transport processes.
  • The study also involved the use of substances known as N-ethylmaleimide (NEM) and calyculin A, which are inhibitors for kinase and phosphatase respectively. These enzymes are known to play roles in the phosphorylation process, which is crucial to the regulation of many biological processes.

Findings of the Study

  • Increased pressure introduced a rise in chloride-dependent potassium transport. However, this effect disappeared when NEM or calyculin A was present, suggesting the hydrostatic pressure effects may be tied to the phosphorylation status of the KCl co-transporter.
  • The introduction of NEM and calyculin A caused the KCl co-transporter to operate at roughly 30% of the maximum flux (rate of transport of ions), compared to when only NEM was present. Similarly, additional pressure did not further affect this operation.
  • The article suggests the implication that hydrostatic pressure impacts not the ion flux itself, but likely the phosphorylation status of the transporter or a regulatory peptide.
  • Furthermore, the pressure-induced activation of the KCl co-transporter appeared to occur without any significant changes to cell volume, bringing implications for any proposed universal model for the regulation of KCl co-transport.

Conclusion

  • This research has offered new insights into the regulation of the KCl co-transporter within horse red blood cells. It highlights the potential significance of hydrostatic pressure and the phosphorylation status of the transporter in the process.
  • The findings could be fundamental in advancing our understanding of how variation in hydrostatic pressure conditions may affect cellular processes, in various fields such as physiology, medicine, and biotechnology.

Cite This Article

APA
Gibson JS, Hall AC. (1995). Stimulation of KCl co-transport in equine erythrocytes by hydrostatic pressure: effects of kinase/phosphatase inhibition. Pflugers Arch, 429(3), 446-448. https://doi.org/10.1007/BF00374163

Publication

ISSN: 0031-6768
NlmUniqueID: 0154720
Country: Germany
Language: English
Volume: 429
Issue: 3
Pages: 446-448

Researcher Affiliations

Gibson, J S
  • Department of Veterinary Preclinical Sciences, University of Liverpool, UK.
Hall, A C

    MeSH Terms

    • Animals
    • Biological Transport, Active / drug effects
    • Biological Transport, Active / physiology
    • Cell Size / drug effects
    • Erythrocytes / drug effects
    • Erythrocytes / metabolism
    • Ethylmaleimide / pharmacology
    • Horses
    • Marine Toxins
    • Oxazoles / pharmacology
    • Phosphoprotein Phosphatases / antagonists & inhibitors
    • Phosphoric Monoester Hydrolases / antagonists & inhibitors
    • Potassium Chloride / blood
    • Pressure
    • Protein Kinase Inhibitors
    • Rubidium Radioisotopes

    Grant Funding

    • Wellcome Trust

    References

    This article includes 8 references
    1. Gibson JS, Ellory JC, Culliford SJ, Fincham DA. Volume-sensitive KCl co-transport and taurine fluxes in horse red blood cells.. Exp Physiol 1993 Sep;78(5):685-95.
    2. Lauf PK, Erdmann A, Adragna NC. K-Cl cotransport, pH, and role of Mg in volume-clamped low-K sheep erythrocytes: three equilibrium states.. Am J Physiol 1994 Jan;266(1 Pt 1):C95-103.
      pubmed: 8304434doi: 10.1152/ajpcell.1994.266.1.C95google scholar: lookup
    3. Cossins AR, Weaver YR, Lykkeboe G, Nielsen OB. Role of protein phosphorylation in control of K flux pathways of trout red blood cells.. Am J Physiol 1994 Dec;267(6 Pt 1):C1641-50.
    4. Dunham PB, Klimczak J, Logue PJ. Swelling activation of K-Cl cotransport in LK sheep erythrocytes: a three-state process.. J Gen Physiol 1993 May;101(5):733-65.
      pubmed: 8336103doi: 10.1085/jgp.101.5.733google scholar: lookup
    5. Lauf PK, Bauer J, Adragna NC, Fujise H, Zade-Oppen AM, Ryu KH, Delpire E. Erythrocyte K-Cl cotransport: properties and regulation.. Am J Physiol 1992 Nov;263(5 Pt 1):C917-32.
    6. Sachs JR, Martin DW. The role of ATP in swelling-stimulated K-Cl cotransport in human red cell ghosts. Phosphorylation-dephosphorylation events are not in the signal transduction pathway.. J Gen Physiol 1993 Sep;102(3):551-73.
      pubmed: 8245823doi: 10.1085/jgp.102.3.551google scholar: lookup
    7. Hall AC, Ellory JC. Effects of high hydrostatic pressure on 'passive' monovalent cation transport in human red cells.. J Membr Biol 1986;94(1):1-17.
      pubmed: 3806656doi: 10.1007/BF01901009google scholar: lookup
    8. Jennings ML, Schulz RK. Swelling-activated KCl cotransport in rabbit red cells: flux is determined mainly by cell volume rather than shape.. Am J Physiol 1990 Dec;259(6 Pt 1):C960-7.

    Citations

    This article has been cited 2 times.
    1. Duan D, Cowley S, Horowitz B, Hume JR. A serine residue in ClC-3 links phosphorylation-dephosphorylation to chloride channel regulation by cell volume.. J Gen Physiol 1999 Jan;113(1):57-70.
      doi: 10.1085/jgp.113.1.57pubmed: 9874688google scholar: lookup
    2. Godart H, Ellory JC. KCl cotransport activation in human erythrocytes by high hydrostatic pressure.. J Physiol 1996 Mar 1;491 ( Pt 2)(Pt 2):423-34.
      doi: 10.1113/jphysiol.1996.sp021226pubmed: 8866865google scholar: lookup