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Journal of Pharmacology And Experimental Therapeutics, Vol. 174, Issue 2, 323-329, 1970
Copyright © 1970 by American Society for Pharmacology and Experimental Therapeutics


ACTIVE TRANSPORT OF Rb86 IN HUMAN RED CELLS AND RAT BRAIN SLICES

J. C. BERNSTEIN 1 and Y. ISRAEL 1

1 Laboratory of General Biochemistry, University of Chile, Santiago, Chile

The use of Rb86 as an analog of K+ was studied in human red cells and in brain cortex slices. In these systems, the uptake of Rb+ was found to follow saturation kinetics. It was demonstrated in red cells that K+ ions produce an inhibition of the competitive type on the uptake of Rb+, a requirement when two substances are transported by the same carrier. Furthermore, the values found for the K1 for K+ and for the Vmax for Rb+ are similar to those described in the literature for the Km(K+) and the Vmax(K+), respectively. Rubidium ions activated the efflux of Na22 from red cells and this effect, as well as the influx of Rb+1 itself, was inhibited by ouabain. In agreement with what has been reported by other authors for K+, sodium ions in the extracellular medium inhibited the uptake of Rb+ when the latter was present in low concentrations (0.2 mM). At higher concentrations of Rb+ (4 mM), Na+ activates the Rb+ uptake. Only part of the Na+-activated influx of Rb+ is inhibited by onabain. The possibility of an influx of Rb+ through pump lB and II is discussed. On the basis of these results it is coneluded that at least 90% of the Rb+ is transported in red cells through mechanisms that have the same characteristics as those that have been described for K+. In rat brain slices, Rb+ was actually accumulated up to 15 times in the tissue. In the presence of ouabain, the intracellular concentration of Rb+ reached a concentration equal to that in the incubation medium. The data presented indicate that Rb86 can be used as an analog of K42 in these systems.

Submitted on December 23, 1969
Accepted on April 20, 1970







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Copyright © 1970 by the American Society for Pharmacology and Experimental Therapeutics.