Passive sodium and potassium movements in sickle erythrocytes.

Abstract

Deoxygenation causes an increase in passive Na and K movements across the membrane of the sickle erythrocyte. Some investigators find that these ion movements are accompanied by cell dehydration, while others find no evidence for cell water loss with sickling. Because gelation of hemoglobin S would be enhanced by cell water loss, we reinvestigated Na and K movements in sickle cells to define further the role that ion movements might play in the pathogenesis of sickling. With deoxygenation, we found that sickle cells gained Na and lost K without losing cell water. These net ion movements were not seen in control red blood cells. For sickle cells, deoxygenation also increased passive unidirectional influxes of Na and K, effects not observed when control red blood cells were deoxygenated. The deoxygenation-induced passive influxes of Na and K in sickle cells were not diminished by anion substitution or by the addition of the diuretic furosemide. We also found differences in passive Na and K fluxes between oxygenated sickle cells and normal red blood cells. The addition of furosemide or replacement of Cl with NO3 or SCN, maneuvers that largely reduced passive Na and K movements in oxygenated normal cells, had no effect on Na and K movements in oxygenated sickle cells. These findings militate against the idea that solute and water loss occur as a consequence of deoxygenation but do indicate that there are acquired membrane abnormalities in sickle red blood cells.