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Calcium accumulated by sickle cell anemia red cells does not affect their
potassium (86Rb+) flux components
OE Ortiz, VL Lew and RM Bookchin
We investigate here the hypothesis that the high Ca content of sickle cell
anemia (SS) red cells may produce a sustained activation of the
Ca2+-dependent K+ permeability (Gardos effect) and that the particularly
high Ca levels in the dense SS cell fraction rich in irreversibly sickled
cells (ISCs) might account for the Na pump inhibition observed in these
cells. We measured active and passive 86Rb+ influx (as a marker for K+) in
density-fractionated SS cells before and after extraction of their excess
Ca by exposure to the Ca ionophore (A23187) and ethylene glycol
tetra-acetic acid and with or without adenosine triphosphate depletion or
addition of quinine. None of these maneuvers revealed any evidence of a
Ca2+-dependent K leak in SS discocytes or dense cells. Na pump inhibition
in the dense SS cells was associated with normal activation by external K+
and a low Vmax that persisted after Ca extraction from the cells. These
results are consistent with our recent findings that the excess Ca in these
cells is compartmentalized in intracellular inside-out vesicles and
unavailable as free Ca2+ to the inner membrane surface. Although the
steady-state free cytoplasmic Ca2+ in oxygenated SS cells must be below the
levels needed to activate the K+ channel, possible brief activation of the
channels of some SS cells resulting from transient elevations of cell Ca2+
during deoxygenation-induced sickling cannot be excluded. The dense,
ISC-rich SS cell fraction showed a Ca2+-independent increase in the
ouabain-resistant, nonsaturable component of 86Rb+ influx that, if
uncompensated by Na+ gain, could contribute to the dehydration of these
cells.
Volume 67,
Issue 3,
pp. 710-715,
03/01/1986
Copyright © 1986 by The American Society of Hematology
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