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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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Article info
Publication history
Accepted:
March 1,
1967
Received:
November 29,
1966
Footnotes
☆Supported in part by the United States Public Health Service Grant HE 08530-03, and Training Grant TL-AM-5241-07, and by the John A. Hartford Foundation.
Identification
Copyright
© 1967 Published by Elsevier Inc.