RESUMEN
Sickle cell have an abnormally high level of calcium and, by an unknown mechanism, exhibit an increase in Caý+ permeability when they are sickled upon deoxygenation. This reversible increase in Caý+ permeability might contribute to cell dehydration by activation of K+ and water loss through the Caý+ permeability might contribute to cell dehydration by activation of K+ and water loss through the Caý+ dependent K+ channel (Gardos pathway). In the present study, the mechanism involved in Ca+ influx stimulation in sickle cells induced by deoxygenation was investigated by three different experiments: Ca2+uptake (1) in the presence of an extracellular impermeant marker to test endocytosis, (2) in the presence of the Caý+uptake (1) in the presence of an extracellular impermeant marker to test endocytosis, (2) in the presence of the Caý= -channel inhibitor Nifedipine, and (3) in the presence of an anion-exchanger inhibitor 4,4' - diisothiocyanatostilbene-2,2' - disulfonic acid (DIDS). These experiments revealed that endocytosis accounted for 6 percent to 19 percent of the Ca2+ uptake in deoxygenated sickle cells a nd that the increased Ca2+ influx was in part blocked by Nifedipine and by DIDS. The present findings, describing different pathways involved in the Caý+ increased permeability of deoxygenated sickle cells are of potential therapeutic interest (AU)