Am J Physiol Cell Physiol AJP: Cell Physiology
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Am J Physiol Cell Physiol 266: C1112-C1117, 1994;
0363-6143/94 $5.00
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AJP - Cell Physiology, Vol 266, Issue 4 C1112-C1117, Copyright © 1994 by American Physiological Society


ARTICLES

Extracellular Mg(2+)-dependent Na+, K+, and Cl- efflux in squid giant axons

H. Rasgado-Flores, H. Gonzalez-Serratos and J. DeSantiago
Department of Physiology and Biophysics, Finch University of Health Sciences, Chicago Medical School, Illinois 60064.

An extracellular Na+ (Nao)-dependent Mg2+ efflux process that requires intracellular ATP has been proposed as the sole mechanism responsible for Mg2+ extrusion in internally dialyzed squid axons (12). We have shown that this exchanger can also "reverse" and mediate an extracellular Mg2+ (Mgo)-dependent Na+ efflux (16). We have extended these studies and found that, in the presence of ouabain, bumetanide, tetrodotoxin, and K+ channel blockers and in the absence of extracellular Na+, K+, and bicarbonate, intracellular K+ and Cl- are also involved in the Mgo-dependent Na+ efflux process. Two main observations support this view: 1) operation of the Mgo-dependent Na+ efflux requires the presence of intracellular K+ and Cl-, and 2) Mgo removal produces a reversible and nearly identical reduction in the magnitude of the simultaneous efflux of the ionic pairs K(+)-Na+ and Cl(-)-Na+. These results suggest that the putative bumetanide-insensitive Na-Mg exchanger also transports K+ and Cl-.


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M. Tashiro and M. Konishi
Sodium gradient-dependent transport of magnesium in rat ventricular myocytes
Am J Physiol Cell Physiol, December 1, 2000; 279(6): C1955 - C1962.
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