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Effect of a 'sickling pulse' on calcium and potassium transport in sickle cell trait red cells.
J Physiol 1981; 312:265-80JP

Abstract

1. To trace the early development of the extensive functional membrane abnormalities found in sickle cell anaemia red cells which result from polymerization of haemoglobin S, we followed the effects on Ca and K transport of an in vitro sickling pulse in sickle cell trait (SA) red cells, whose membranes are initially normal.2. Sickling induced a progressively larger uptake of Ca in fed, starved and ATP-depleted SA cells, always substantially higher than that in normal (AA) red cells under comparable conditions. The fraction of ionized Ca within the SA cells, estimated from the equilibrium distribution of (45)Ca induced by the ionophore A23187 was about 0.4 of the total Ca content and similar in SA and AA cells.3. With ATP-depleted SA cells, Ca uptake (representing Ca permeability) was maximal during sickling and was only partially reduced towards normal after desickling. Net Ca uptake during sickling of fed or starved SA cells reverted to net Ca loss upon reoxygenation, irrespective of the Ca gradient, indicating full restoration of the low Ca permeability of the control conditions.4. Following desickling of both fed and starved SA cells, the rates of uphill extrusion of Ca gained during sickling were much smaller than those expected with normal Ca pumps operating at similar internal Ca concentrations.5. After 2 hr sickling ATP levels in starved SA cells were reduced by 50% regardless of the presence or absence of Ca in the medium; therefore sickling-induced Ca uptake was associated with no measurable consumption of ATP due to Ca-pump activity.6. With ATP-depleted SA cells, a Ca uptake of 2-3 mumole/l. cells elicited a maximal response of the K permeability system resulting in full equilibration of the K pools in the cell suspensions. Sickling of fed and starved SA cells produced a small increase in K permeability which was entirely independent of the presence or absence of Ca.7. Sickled forms persisted after reoxygenation only with ATP-depleted SA cells and were more frequent after sickling in the presence of Ca (about 20%) than in a Ca-free medium (about 4%).8. These findings show that initial sickling produces an increased Ca permeability whose extent and reversibility depends on the metabolic state of the cells, and a partial Ca-pump failure, which appears to be irreversible. We confirm a small sickling-related, reversible increase in K permeability but a Ca-dependent increase in K permeability does not occur unless the cells are fully depleted of ATP. The implications for sequential development of related abnormalities in SS cells are discussed.

Authors

No 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

7264994

Citation

Bookchin, R M., and V L. Lew. "Effect of a 'sickling Pulse' On Calcium and Potassium Transport in Sickle Cell Trait Red Cells." The Journal of Physiology, vol. 312, 1981, pp. 265-80.
Bookchin RM, Lew VL. Effect of a 'sickling pulse' on calcium and potassium transport in sickle cell trait red cells. J Physiol (Lond). 1981;312:265-80.
Bookchin, R. M., & Lew, V. L. (1981). Effect of a 'sickling pulse' on calcium and potassium transport in sickle cell trait red cells. The Journal of Physiology, 312, pp. 265-80.
Bookchin RM, Lew VL. Effect of a 'sickling Pulse' On Calcium and Potassium Transport in Sickle Cell Trait Red Cells. J Physiol (Lond). 1981;312:265-80. PubMed PMID: 7264994.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of a 'sickling pulse' on calcium and potassium transport in sickle cell trait red cells. AU - Bookchin,R M, AU - Lew,V L, PY - 1981/3/1/pubmed PY - 1981/3/1/medline PY - 1981/3/1/entrez SP - 265 EP - 80 JF - The Journal of physiology JO - J. Physiol. (Lond.) VL - 312 N2 - 1. To trace the early development of the extensive functional membrane abnormalities found in sickle cell anaemia red cells which result from polymerization of haemoglobin S, we followed the effects on Ca and K transport of an in vitro sickling pulse in sickle cell trait (SA) red cells, whose membranes are initially normal.2. Sickling induced a progressively larger uptake of Ca in fed, starved and ATP-depleted SA cells, always substantially higher than that in normal (AA) red cells under comparable conditions. The fraction of ionized Ca within the SA cells, estimated from the equilibrium distribution of (45)Ca induced by the ionophore A23187 was about 0.4 of the total Ca content and similar in SA and AA cells.3. With ATP-depleted SA cells, Ca uptake (representing Ca permeability) was maximal during sickling and was only partially reduced towards normal after desickling. Net Ca uptake during sickling of fed or starved SA cells reverted to net Ca loss upon reoxygenation, irrespective of the Ca gradient, indicating full restoration of the low Ca permeability of the control conditions.4. Following desickling of both fed and starved SA cells, the rates of uphill extrusion of Ca gained during sickling were much smaller than those expected with normal Ca pumps operating at similar internal Ca concentrations.5. After 2 hr sickling ATP levels in starved SA cells were reduced by 50% regardless of the presence or absence of Ca in the medium; therefore sickling-induced Ca uptake was associated with no measurable consumption of ATP due to Ca-pump activity.6. With ATP-depleted SA cells, a Ca uptake of 2-3 mumole/l. cells elicited a maximal response of the K permeability system resulting in full equilibration of the K pools in the cell suspensions. Sickling of fed and starved SA cells produced a small increase in K permeability which was entirely independent of the presence or absence of Ca.7. Sickled forms persisted after reoxygenation only with ATP-depleted SA cells and were more frequent after sickling in the presence of Ca (about 20%) than in a Ca-free medium (about 4%).8. These findings show that initial sickling produces an increased Ca permeability whose extent and reversibility depends on the metabolic state of the cells, and a partial Ca-pump failure, which appears to be irreversible. We confirm a small sickling-related, reversible increase in K permeability but a Ca-dependent increase in K permeability does not occur unless the cells are fully depleted of ATP. The implications for sequential development of related abnormalities in SS cells are discussed. SN - 0022-3751 UR - https://www.unboundmedicine.com/medline/citation/7264994/Effect_of_a_'sickling_pulse'_on_calcium_and_potassium_transport_in_sickle_cell_trait_red_cells_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0022-3751&date=1981&volume=312&spage=265 DB - PRIME DP - Unbound Medicine ER -