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Am J Physiol Cell Physiol 269: C403-C409, 1995;
0363-6143/95 $5.00
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AJP - Cell Physiology, Vol 269, Issue 2 C403-C409, Copyright © 1995 by American Physiological Society

ARTICLES

Deoxygenation-induced cation fluxes in sickle cells. IV. Modulation by external calcium

C. H. Joiner, M. Jiang and R. S. Franco
Department of Pediatrics, University of Cincinnati College of Medicine, Children's Hospital Medical Center, Ohio, USA.

Net cation movements were measured in low-density sickle red blood cells (SS RBC) in the presence and absence of oxygen. External Ca2+ (Ca2+o) partially inhibited deoxygenation-induced fluxes of both Na+ and K+. Deoxygenation-induced Na+ influx was reduced by 2 mM Ca2+o to 0.71 +/- 0.04 (SE) of its value in Ca(2+)-free solutions, whereas this ratio was 0.90 +/- 0.05 for K+ efflux (P < 0.01 by paired t-test). Because Ca2+o inhibited Na+ influx more than K+ efflux, net cation loss in deoxygenated SS RBC was higher in the presence of Ca2+o. In separate experiments, Ca2+o reduced deoxygenation-induced Na+ influx to 0.66 +/- 0.03 of its Ca(2+)-free value compared with 0.77 +/- 0.03 for Rb+ influx (P < 0.001), indicating relative selectivity of this effect for Na+ over Rb+. However, this effect is not specific for Ca2+ because other divalent cations also inhibited deoxygenation-induced Na+ and K+ fluxes. Under the conditions of these experiments, no evidence for K+ channel activation was found, indicating that K+ loss measured in deoxygenated SS RBC was mediated by the deoxygenation-induced pathway. These studies show that in the presence of Ca2+o deoxygenation-induced Na+ influx and K+ efflux are unbalanced. This pathway can, therefore, mediate cation loss and contribute directly to cellular dehydration in SS RBC.


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