Calcium-induced potassium pathway in sided erythrocyte membrane vesicles.
We have characterized the asymmetric effect of Ca2+ on passive K+ permeability in erythrocyte membranes, using inside out and right-side out vesicles. Ca2+, but not Mg2+, can induce an increase in K+ uptake in inside out vesicles. The half-maximal concentration of Ca2+ required to induce the K+ uptake is 0.2 mM, and the permeability increase is not specific for K+. Thus, the Ca2+- induced permeation process in inside out vesicles is changed from that in the energy-depleted intact cell which requires only micromolar concentrations of Ca2+ and is specific for K+. Removal of spectrin had no effect on the vesicle permeability increase due to Ca2+. Studies with N-ethylmaleimide  show that the vesicle channel openings is mediated by a protein and passage is controlled by sulfhydryl groups; furthermore, the Ca2+-induced vesicle pathway is distinct from the normal channel for passive K+ leak in the absence of Ca2+. The protein is sensitive to its phospholipid environment since removal of easily accessible phospholipid head groups on the cytoplasmic face of the vesicles inhibits the Ca2+ -stimulated channel opening.
D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D004912:Erythrocytes / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D007700:Kinetics; D008274:Magnesium / Q000494:pharmacology; D010539:Permeability; D011188:Potassium / Q000097:blood*; D012413:Rubidium / Q000097:blood
D007473:Ion Channels; D008274:Magnesium; D012413:Rubidium; D011188:Potassium; D002118:Calcium