Passive Ca2+ transport and Ca2+-dependent K+ transport in Plasmodium falciparum-infected red cells

Previous reports have indicated that Plasmodium falciparum-infected red cel ls (pRBC) have an increased Ca2+ permeability. The magnitude of the increas e is greater than that normally required to activate the Ca2+-dependent Kchannel (K-Ca channel) of the red cell membrane. However, there is evidence that this channel remains inactive in pRBC. To clarify this discrepancy, w e have reassessed both the functional status of the K-Ca channel and the Ca 2+ permeability properties of pRBC. For pRBC suspended in media containing Ca2+, K-Ca channel activation was elicited by treatment with the Ca2+ ionop hore 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 n ormal range (30-55 mu mol (10(13) cells . hr)(-1)), provided the cells were suspended in glucose-containing media. However, for pRBC in glucose-free m edia the Ca2+ influx increased to over 1 mmol (1013 cells . hr)(-1), almost an order of magnitude higher than that seen in uninfected erythrocytes und er equivalent conditions. The pathway responsible for the enhanced influx o f Ca2+ into glucose-deprived pRBC was expressed at approximately 30 hr post -invasion, and was inhibited by Ni2+. Possible roles for this pathway in pR BC are considered.