The increased K⁺ leak of malaria-infected erythrocytes is not via a Ca²⁺-activated K⁺ channel

Charybdotoxin and nitrendipine both inhibited K⁺ (⁸⁶Rb⁺) influx via the Ca²⁺-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 Ca²⁺-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.