sq-23377 and Malaria--Falciparum

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.

Topics: Animals; Charybdotoxin; Erythrocytes; Humans; Ionomycin; Kinetics; Malaria, Falciparum; Nitrendipine; Plasmodium falciparum; Potassium; Potassium Channels; Rubidium; Scorpion Venoms