title: Stimulation of Na+/Mg2+ antiport in rat erythrocytes by intracellular Cl-.
abstract: Mg(2+) efflux from rat erythrocytes was measured in NaCl, NaNO(3), NaSCN and Na gluconate medium. Substitution of extracellular and intracellular Cl(-) with the permeant anions NO(3)(-) and SCN(-) reduced Mg(2+) efflux via Na(+)/Mg(2+) antiport. After substitution of extracellular Cl(-) with the non-permeant anion gluconate, Mg(2+) efflux was not significantly reduced. In Na gluconate medium, an influence of the changed membrane potential and intracellular pH on Mg(2+) efflux could be excluded. The results indicate the existence of Cl(-)-independent Na(+)/Mg(2+) antiport and of Na(+)/Mg(2+) antiport stimulated by intracellular Cl(-). Intracellular Cl(-), as determined by means of (36)Cl(-), was found to stimulate Na(+)/Mg(2+) antiport through a cooperative effect according to a sigmoidal kinetics. The Hill coefficient for intracellular Cl(-) amounted to 1.4-1.8, indicating that two intracellular Cl(-) may be simultaneously active. With respect to specificity, Cl(-) was most effective, followed by Br(-), J(-), and F(-). Stimulation of Na(+)/Mg(2+) antiport by intracellular Cl(-) together with intracellular Mg(2+) may play a role during deoxygenation of erythrocytes and in essential hypertension.
authors.affiliation: Institut für Klinische Physiologie, Klinikum Benjamin Franklin, Freie Universität Berlin, Hindenburgdamm 30, 12200, Berlin, Germany. hans.ebel@medizin.fu-berlin.de
authors.forename: H
authors.initials: H
authors.lastname: Ebel
authors.forename: T
authors.initials: T
authors.lastname: Günther
mesh_terms: D000818:Animals; D017920:Antiporters / Q000378:metabolism*; D002712:Chlorides / Q000494:pharmacology / Q000502:physiology*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D017136:Ion Transport / Q000187:drug effects; D007700:Kinetics; D008274:Magnesium / Q000378:metabolism; D051381:Rats
chemical_list: D017920:Antiporters; D002712:Chlorides; C046250:sodium-magnesium antiporter; D008274:Magnesium