Ca2+ permeability in deoxygenated sickle cells.
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.
Rhoda
M D
MD
INSERM CIF 8814, Centre hospitalier, Pointe-à-Pitre, Guadeloupe, France.
Apovo
M
M
Beuzard
Y
Y
Giraud
F
F
D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D000755:Anemia, Sickle Cell / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000097:blood*; D015220:Calcium Channels / Q000502:physiology; D002463:Cell Membrane Permeability / Q000187:drug effects; D004705:Endocytosis; D004910:Erythrocyte Membrane / Q000502:physiology*; D006801:Humans; D009543:Nifedipine / Q000494:pharmacology; D010100:Oxygen / Q000097:blood
D015220:Calcium Channels; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D009543:Nifedipine; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D010100:Oxygen; D002118:Calcium