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PubMed · 2161689

Ca2+ permeability in deoxygenated sickle cells.

M D Rhoda·M Apovo·Y Beuzard·F Giraud
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Abstract

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.

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4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAnemia, Sickle CellBiological TransportCalciumCalcium ChannelsCell Membrane PermeabilityEndocytosisErythrocyte MembraneHumansNifedipineOxygenJournal ArticleResearch Support, Non-U.S. Gov't

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M D Rhoda, M Apovo, Y Beuzard, F Giraud. 1990-06-15. Ca2+ permeability in deoxygenated sickle cells.. https://pubmed.ncbi.nlm.nih.gov/2161689/

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