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1 Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada N6A 5C1; and 2 Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, St. Louis, Missouri 63104
The release of ATP from red
blood cells (RBC) in response to low O2 levels is linked to
ATP production and the oxygenation state of hemoglobin. Because
O2 is unloaded from the RBC, the concentration of
deoxygenated hemoglobin increases, displacing phosphofructokinase from
the cytoplasmic domain of band 3. We hypothesize that the ATP molecules
produced through this glycolytic stimulation at the membrane surface
result in the release of ATP from the RBC. Rat whole blood exposed to 5 min of low PO2 in vitro increased plasma
[ATP] by 1.0 µM (+45%). This increase was reduced to 0.1 µM
(+12%, P < 0.05) after citrate incubation and
reversed after fluoride treatment (both glycolytic inhibitors) by 
0.2 µM (23%, P < 0.05). Plasma [ATP] of control RBC
decreased 0.3 µM (12%) when 8% CO (P < 0.05)
was added to the chamber. Because CO and O2 bind
competitively to heme, these results support our hypothesis that the
release of ATP from RBC is linked to ATP production through the
oxygenation state of the hemoglobin molecule.
adenosine triphosphate; O2 regulation; glycolysis; microcirculation; membrane transport
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