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Calcium accumulated by sickle cell anemia red cells does not affect their potassium (86Rb+) flux components.
Blood 1986; 67(3):710-5Blood

Abstract

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.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2418897

Citation

Ortiz, O E., et al. "Calcium Accumulated By Sickle Cell Anemia Red Cells Does Not Affect Their Potassium (86Rb+) Flux Components." Blood, vol. 67, no. 3, 1986, pp. 710-5.
Ortiz OE, Lew VL, Bookchin RM. Calcium accumulated by sickle cell anemia red cells does not affect their potassium (86Rb+) flux components. Blood. 1986;67(3):710-5.
Ortiz, O. E., Lew, V. L., & Bookchin, R. M. (1986). Calcium accumulated by sickle cell anemia red cells does not affect their potassium (86Rb+) flux components. Blood, 67(3), pp. 710-5.
Ortiz OE, Lew VL, Bookchin RM. Calcium Accumulated By Sickle Cell Anemia Red Cells Does Not Affect Their Potassium (86Rb+) Flux Components. Blood. 1986;67(3):710-5. PubMed PMID: 2418897.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcium accumulated by sickle cell anemia red cells does not affect their potassium (86Rb+) flux components. AU - Ortiz,O E, AU - Lew,V L, AU - Bookchin,R M, PY - 1986/3/1/pubmed PY - 1986/3/1/medline PY - 1986/3/1/entrez SP - 710 EP - 5 JF - Blood JO - Blood VL - 67 IS - 3 N2 - 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. SN - 0006-4971 UR - https://www.unboundmedicine.com/medline/citation/2418897/Calcium_accumulated_by_sickle_cell_anemia_red_cells_does_not_affect_their_potassium__86Rb+__flux_components_ L2 - http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=2418897 DB - PRIME DP - Unbound Medicine ER -