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.
Kirk
K
K
University Laboratory of Physiology, Oxford, UK.
Elford
B C
BC
Ellory
J C
JC
D000818:Animals; D018999:Charybdotoxin; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism* / Q000469:parasitology; D006801:Humans; D015759:Ionomycin / Q000494:pharmacology; D007700:Kinetics; D016778:Malaria, Falciparum / Q000097:blood*; D009568:Nitrendipine / Q000494:pharmacology; D010963:Plasmodium falciparum / Q000472:pathogenicity; D011188:Potassium / Q000097:blood*; D015221:Potassium Channels / Q000378:metabolism*; D012413:Rubidium / Q000097:blood; D012604:Scorpion Venoms / Q000494:pharmacology
D015221:Potassium Channels; D012604:Scorpion Venoms; D018999:Charybdotoxin; D015759:Ionomycin; D009568:Nitrendipine; D012413:Rubidium; D011188:Potassium