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

WITH sickle cell disease, certain subsets of red blood (SS RBC) exhibit depletion and cellular dehydration (12-15, 21, 22). The resultant increase in hemoglobin concentration greatly accelerates the rate of polymerization of hemoglobin S (HbS) on deoxygenation (11). In animal models, dense sickle are selectively trapped in the peripheral vasculature and mediate vasoocclusion (12, 27), and in sickle cell patients the dense cell fraction is selectively lost during clinical pain episodes (1, 12). Thus cellular dehydration appears to contribute to the pathophysiology of the sickling syndromes (2 1). Three transport pathways are considered potential mediators of SS RBC dehydration in vivo: 1) a deoxygenation-induced pathway mediating passive of Na+ and K+ as well as and Mg2+; 2) the -dependent K+ channel, activated by deoxygenation-induced influx; and 3) the K-Cl cotransporter. High levels of K-Cl cotransport can be demonstrated in SS RBC (7,8); the cotransporter can be activated in oxygenated SS RBC by relatively mild acidic conditions that may prevail in part of the circulation (7), but it is inhibited by deoxygenation (8). Recent data from our laboratory 0363-6143/95 $3.00 Copyright o 1995 suggest that K-Cl cotransport may mediate the deoxygenation-independent dehydration of some SS RBC reticulocytes (15). The http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Cell Physiology The American Physiological Society

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