Abstract
The mechanism of the "ground permeability" of the human erythrocyte membrane for K+ and Na+ was investigated with respect to a possible involvement of a previously unidentified specific transport pathway, because earlier studies showed that it cannot be explained on the basis of simple electrodiffusion. In particular, we analyzed and described the increase in the (ouabain+bumetanide+EGTA)-insensitive unidirectional K+ and Na+ influxes as well as effluxes (defined as "leak" fluxes) observed in erythrocytes suspended in low-ionic-strength media. Using a carrier-type model and taking into account the influence of the ionic strength on the outer surface potential according to the Gouy-Chapman theory (i.e., the ion concentration near the membrane surface), we are able to describe the altered "leak" fluxes as an electroneutral process. In addition, we can show indirectly that this electroneutral flux is due to an exchange of monovalent cations with protons. This pathway is different from the amiloride-sensitive Na+/H+ exchanger present in the human red blood cell membrane and can be characterized as a K+(Na+)/H+ exchanger.
MeSH Terms
Binding Sites
Bumetanide/pharmacology
Cations, Monovalent/blood
Egtazic Acid/pharmacology
Erythrocyte Membrane/drug effects,metabolism
Erythrocytes/drug effects,metabolism
Humans
In Vitro Techniques
Kinetics
Membrane Potentials
Models, Biological
Osmolar Concentration
Ouabain/pharmacology
Potassium/blood
Sodium/blood
Sodium-Hydrogen Exchangers/blood
Chemicals
Cations, Monovalent
Sodium-Hydrogen Exchangers
Bumetanide
Egtazic Acid
Ouabain
Sodium
Potassium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Richter S
Biophysics Section, Humboldt University Berlin, Germany.
Hamann J
Kummerow D
Bernhardt I
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