Vanadium increases selective K+-permeability in human erythrocytes.
In human erythrocytes that had been depleted of ATP by incubation with iodoacetate and adenosine, vanadate induces a 10-15-fold increase of K+-permeability. The effect is similar to that produced by calcium ions. Like the calcium-induced permeability change, the vanadate-induced effect is preceded by a lag period. Preincubation without substrates for ATP synthesis reduces the length of the lag period following the addition of either vanadate or calcium. The selective change of K+-permeability was brought about by vanadate anions (+5 oxidation state) as well as by vanadyl cations (+4 oxidation state). In both cases, the presence of EDTA prevented the permeability change. Blocking of the anion-transport system of the human erythrocytes by H2DIDS was used to discriminate between the unstable forms of vanadate anion and vanadyl cation in producing the potassium loss. The observation that H2DIDS had little if any effect on the efficiency and the previously reported fact by Cantley, L.C. and Aisen, Ph. (J. Biol. Chem., 254 (1979) 1781) that vanadate appears mostly as vanadyl in the cell interior suggests that, similar to Ca2+, Mg2+ or Pb2+, vanadyl (VO2+) can open the "potassium channel" in the erythrocyte membrane.
D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007461:Iodoacetates / Q000494:pharmacology; D010539:Permeability; D011188:Potassium / Q000378:metabolism*; D014639:Vanadium / Q000494:pharmacology*
D007461:Iodoacetates; D014639:Vanadium; D011188:Potassium