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Research Article| Volume 70, ISSUE 1, P69-79, July 1967

Potassium transport in human blood platelets

  • Mark H. Cooley
    Affiliations
    From the Richard C. Curtis Hematology Laboratory and the Department of Medicine, Peter Bent Brigham Hospital, Boston, Mass. U.S.A.

    From the Department of Medicine, Harvard Medical School Boston, Mass. U.S.A.
    Search for articles by this author
  • Phin Cohen
    Affiliations
    From the Richard C. Curtis Hematology Laboratory and the Department of Medicine, Peter Bent Brigham Hospital, Boston, Mass. U.S.A.

    From the Department of Medicine, Harvard Medical School Boston, Mass. U.S.A.
    Search for articles by this author
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      Abstract

      Potassium transport mechanisms in fresh human blood platelets have been investigated, and the results suggest a similarity to erythrocyte potassium flux kinetics. The influx of potassium into platelets appears to be a two component system, having a “pump” flux component, dependent on glucose, and a linear or “leak” component, dependent on the concentration of potassium in the suspending medium. In the absence of potassium, platelets cannot maintain a normal potassium concentration. Glucose provides the high-energy phosphate (ATP), via glycolytic pathways, without which platelets cease to actively bind potassium. Inhibition of glycolysis with iodoacetate or sodium fluoride resulted in a marked suppression of potassium influx. At high concentrations of sodium fluoride there was an increased leak of potassium from platelets, which was further augmented by addition of calcium to the medium. Simultaneous with sodium fluoride induced inhibition of potassium influx rate, platelet ATP concentraton fell to nearly zero. Ouabain, however, inhibited platelet potassium influx without affecting platelet glycolysis.
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