Extracellular Mg(2+)-dependent Na+, K+, and Cl- efflux in squid giant axons.
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-.
Rasgado-Flores
H
H
Department of Physiology and Biophysics, Finch University of Health Sciences, Chicago Medical School, Illinois 60064.
Gonzalez-Serratos
H
H
DeSantiago
J
J
D000818:Animals; D017920:Antiporters / Q000378:metabolism; D001369:Axons / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism*; D049832:Decapodiformes; D005110:Extracellular Space / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*
D017920:Antiporters; D002712:Chlorides; C046250:sodium-magnesium antiporter; D012964:Sodium; D008274:Magnesium; D011188:Potassium