Chloride-activated passive potassium transport in human erythrocytes.
Passive K+ transport in human erythrocytes (defined as ouabain-insensitive transport) was inhibited 70% by replacement of Cl- by several permeant monovalent anions. The Vmax of Cl--dependent K+ influx was 1.14 mmol . liter-1, hr-1; its apparent Km for K+ was 4.7 mM. There was a much smaller component of Na+ influx dependent on Cl- (Vmax, 0.23 mmol . liter-1 . hr-1). Furosemide and other inhibitors of Cl- transport inhibited passive K+ transport to the same extent as replacement of Cl-, but 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, a specific inhibitor of anion exchange in erythrocytes, was ineffective. The Cl--dependent K+ transport, which may be K+/Cl- cotransport, could reflect a mechanism for regulating cell volume.
D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000328:Adult; D001692:Biological Transport / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000097:blood / Q000494:pharmacology*; D004910:Erythrocyte Membrane / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism*; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000097:blood*; D012964:Sodium / Q000097:blood
D002712:Chlorides; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D011188:Potassium