AJP - Cell Physiology, Vol 259, Issue 4 C541-C548, Copyright © 1990 by American Physiological Society
Extracellular magnesium-dependent sodium efflux in squid giant axons
H. Gonzalez-Serratos and H. Rasgado-Flores
Department of Biophysics, University of Maryland Medical School, Baltimore 21201.
Experiments were designed to determine whether the putative Na(+)-Mg2+
exchanger previously demonstrated to mediate Mg2+ efflux (R. DiPolo and L.
Beague. Biochim. Biophys. Acta 946: 424-428, 1988) could also mediate the
efflux of Na+ (presumably a Na+ efflux-Mg2+ influx exchange) in squid giant
axons. The effects of external Mg2+ (Mg(o)) on 22Na efflux were measured in
internally dialyzed, ATP-fueled axons in which the contribution to Na+
efflux by other pathways was inhibited. To facilitate measurement of
Mg(o)-dependent Na+ efflux, the intracellular concentration of Na+ was
increased. To prevent Na(+)-Na+ exchange, external Na+ was replaced by
tris(hydroxymethyl)aminomethane. To assess the effect of Mg(o) on Na+
efflux without altering the total divalent cation concentrations, Mg(o) was
replaced mole-for-mole by external Ba2+ (Ba(o)). This manipulation produced
reversible reductions in Na+ efflux. These reductions were neither due to
membrane hyperpolarization nor to a direct effect of Bao but were due
instead to the reduction in Mg(o). The Mg(o)-dependent Na+ efflux was
inhibited by external amiloride but was spared by bumetanide. In the
absence of external Na+, the Mgo-dependent Na+ efflux increased as a
function of external Mg2+ with Michaelis-Menten kinetics. These results
indicate that the Na(+)-Mg2+ exchange can mediate the efflux of Na+
(operate in Na+ efflux-Mg2+ influx mode of exchange).
