Ca2+ permeability in deoxygenated sickle cells
MD Rhoda, M Apovo, Y Beuzard and F Giraud
INSERM CIF 8814, Centre hospitalier, Pointe-a-Pitre, Guadeloupe, France.
Deoxygenation of sickle cells is known to increase cation permeabilities
(Na+, K+, and Ca2+). The possible mechanisms involved in the increased
uptake of Ca2+ were investigated: activation of Ca2+ channels, involvement
of the anion channel, and the formation of endocytic vacuoles. The Ca2+
channel blocker nifedipine reduced the deoxy-stimulated Ca2+ uptake by
about 30% to 40%. The anion channel inhibitor DIDS (4,4' diisothiocyanate
stilbene 2,2' disulfonate) inhibited the deoxy-stimulated Ca2+ uptake by
approximately 50%. Maximal possible endocytic uptake, measured by using an
impermeant marker ([3H] inuline), accounted for 6% to 9% of the total Ca2+
uptake. These data indicate that the deoxygenation-induced increase in Ca2+
permeability could result from both the activation of a Ca2+ channel and of
a transport system for cations involving interactions between polymerized
hemoglobin S, band 3 and other membrane components. Endocytosis appears to
play only a minor role in the Ca2+ uptake of deoxygenated sickle cells.
Volume 75,
Issue 12,
pp. 2453-2458,
06/15/1990
Copyright © 1990 by The American Society of Hematology
