M. Apovo et al., THE INVOLVEMENT OF THE CA-DEPENDENT K-CHANNEL AND OF THE KCL COTRANSPORT IN SICKLE-CELL DEHYDRATION DURING CYCLIC DEOXYGENATION, Biochimica et biophysica acta. Molecular basis of disease, 1225(3), 1994, pp. 255-258
We have investigated the mechanisms involved in sickle cell dehydratio
n upon continuous or cyclic deoxygenation: the Ca2+-actived K+ channel
and the KCl co-transport system. Short-term continuous deoxygenation
(1 h) of sickle cells in a Ca2+-containing medium promoted a stimulati
on of the efflux of K+ and cell dehydration. This latter was reduced b
y the replacement of Ca2+ in the medium by EGTA, but not by addition o
f [(dihydro indenyl)oxy] alkanoic acid (DIOA), an inhibitor of the KCl
co-transport. During cycles of deoxygenation-reoxygenation, cell dehy
dration was partly prevented by EGTA and significantly reduced by DIOA
only in the presence of Ca2+. The present data support the view that
sickle cell dehydration during deoxygenation arises from the stimulati
on of the Ca2+-dependent K+ permeability leading to water loss, wherea
s during reoxygenation periods, subsequent activation of the KCl co-tr
ansport also contributes to cell dehydration.