The increased K+ leak of malaria-infected erythrocytes is not via a Ca(2+)-activated K+ channel.

Charybdotoxin and nitrendipine both inhibited K+(86Rb+) influx via the Ca(2+)-activated channel of uninfected erythrocytes but had no effect on K+(86Rb+) transport in malaria-infected cells. Activation of the channel in uninfected cells in which the cytoplasmic [Na+]/[K+] ratio was adjusted to be comparable with that of late-stage malaria-infected erythrocytes resulted in a large (nitrendipine-sensitive) increase in K+(86Rb+) influx. These results suggest that the endogenous Ca(2+)-activated K+ channel remains inactive in human red cells infected with late-stage parasites. The identity of the pathway which mediates the increased K(+)-leak in infected erythrocytes remains to be established.