Passive Ca2+ Transport and Ca2+-Dependent K+ Transport in Plasmodium falciparum-Infected Red Cells

Passive Ca2+ Transport and Ca2+-Dependent K+ Transport in Plasmodium falciparum-Infected Red Cells Previous reports have indicated that Plasmodium falciparum-infected red cells (pRBC) have an increased Ca2+ permeability. The magnitude of the increase is greater than that normally required to activate the Ca2+-dependent K+ channel (K Ca channel) of the red cell membrane. However, there is evidence that this channel remains inactive in pRBC. To clarify this discrepancy, we have reassessed both the functional status of the K Ca channel and the Ca2+ permeability properties of pRBC. For pRBC suspended in media containing Ca2+, K Ca channel activation was elicited by treatment with the Ca2+ ionophore A23187. In the absence of ionophore the channel remained inactive. In contrast to previous claims, the unidirectional influx of Ca2+ into pRBC in which the Ca2+ pump was inhibited by vanadate was found to be within the normal range (30–55 μmol (1013 cells · hr)−1), provided the cells were suspended in glucose-containing media. However, for pRBC in glucose-free media the Ca2+ influx increased to over 1 mmol (1013 cells · hr)−1, almost an order of magnitude higher than that seen in uninfected erythrocytes under equivalent conditions. The pathway responsible for the enhanced influx of Ca2+ into glucose-deprived pRBC was expressed at approximately 30 hr post-invasion, and was inhibited by Ni2+. Possible roles for this pathway in pRBC are considered. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Passive Ca2+ Transport and Ca2+-Dependent K+ Transport in Plasmodium falciparum-Infected Red Cells

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 1999 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002329900579
Publisher site
See Article on Publisher Site

Abstract

Previous reports have indicated that Plasmodium falciparum-infected red cells (pRBC) have an increased Ca2+ permeability. The magnitude of the increase is greater than that normally required to activate the Ca2+-dependent K+ channel (K Ca channel) of the red cell membrane. However, there is evidence that this channel remains inactive in pRBC. To clarify this discrepancy, we have reassessed both the functional status of the K Ca channel and the Ca2+ permeability properties of pRBC. For pRBC suspended in media containing Ca2+, K Ca channel activation was elicited by treatment with the Ca2+ ionophore A23187. In the absence of ionophore the channel remained inactive. In contrast to previous claims, the unidirectional influx of Ca2+ into pRBC in which the Ca2+ pump was inhibited by vanadate was found to be within the normal range (30–55 μmol (1013 cells · hr)−1), provided the cells were suspended in glucose-containing media. However, for pRBC in glucose-free media the Ca2+ influx increased to over 1 mmol (1013 cells · hr)−1, almost an order of magnitude higher than that seen in uninfected erythrocytes under equivalent conditions. The pathway responsible for the enhanced influx of Ca2+ into glucose-deprived pRBC was expressed at approximately 30 hr post-invasion, and was inhibited by Ni2+. Possible roles for this pathway in pRBC are considered.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Nov 1, 1999

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