Abstract

Dehydration of sickle red blood cells (SSRBC) is an important pathophysiologio determinant. We have recently shown that the increase in sodium (Na) and potassium (K) permeability which occurs on deoxygenation of SSRBC (but not normal RBC) can contribute to dehydration, despite the balanced ratio of this cation leak. We measured net cation movements in SSRBC incubated in phosphate buffered saline with 0.1 mM ouabain. The “deoxy” fluxes of Na and K were defined by the difference in ion movements in cells equilibrated with 100% N2, vs. 21% 02. The deoxy fluxes of both Na and K were maximal at pH 7.4 - 7.5, and the ratio of deoxy Na influx to deoxy K efflux remained one, over pH 7.0 - 7.9. The increase in ion permeability in SSRBC occurred less than 10 min. after deoxygenation. Similarly, SSRBC cation fluxes returned to baseline within 10 min. upon reoxygenation. Deoxy cation fluxes were activated at pO2, levels of 30 to 45 torr., with both deoxy Na influx and deoxy K efflux showing similar pO2 dependence. These data demonstrate that the increased cation permeability triggered by deoxygenation of SSRBC occurs at physiologic pH and pO2, is rapid in onset and readily reversible. Futhermore, modulation of this transport system by pH and pO2 leads to parallel changes in both Na and K permability. These results suggest that deoxy Na/K fluxes are activated in vivo, and support the involvement of this phenomenon in the process of cellular dehydration of SSRBC.

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