Kirk, KiaranAshworth, Kevin J.Elford, Barry C.Pinches, Robert A.Clive Ellory, J.2025-12-312025-12-310005-2736PubMed:1998699ORCID:/0000-0002-5613-2622/work/162953224https://hdl.handle.net/1885/733797675Human red cells infected in vitro with Plasmodium falciparum showed a significant increase in the rate of both ouabain-sensitive and aouabain-insensitive 86Rb+ influx. The inrease in ouabain-insensitive 86Rb+ influx was due, in part, increased transport via a bumetanide-sensitive system and, in part to transport via a pathway that was absent (or at least inactive) in uninfected cells. The parasite-induced pathway was inhibited by piperine and had a dose response very similar to that of the Gardo's channel of uninfected cells but was less sensitive than the Gardos channel to inhibition by quinine.4en(Human erythrocyte)(P. faiciparum)Infected erythrocyteRubidium-86 transport1991-01-3010.1016/0005-2736(91)90296-K0026433784