In squid axons intracellular Mg2+ is essential for ATP-dependent Na+ efflux in the absence and presence of strophanthidin.
The effect on Na+ efflux of removal of intracellular Mg2+ was studied in squid giant axons dialyzed without internal Ca2+. In the absence of Mg2i+, ATP was unable to stimulate any efflux of Na+ above the baseline of about 1 pmol . cm-2 . s-1. This behavior was observed in otherwise normal axons and in axons poisoned with 50 microM strophanthidin in the sea water. Reinstatement of 4 mM MgCl2 in excess to ATP in the dialysis solution brought about the usual response of Na+ efflux to ATP, external K+ and strophanthidin. The present experiments show that, regardless of the mechanism for the ATP-dependent Na+ efflux in strophanthidin-poisoned axons, this type of flux shares with the active Na+ extrusion the need for the simultaneous presence of intracellular ATP and Mg2+.
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism*; D049832:Decapodiformes; D004533:Egtazic Acid / Q000494:pharmacology; D007700:Kinetics; D008274:Magnesium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D013327:Strophanthidin / Q000494:pharmacology*
D004533:Egtazic Acid; D013327:Strophanthidin; D000255:Adenosine Triphosphate; D012964:Sodium; D008274:Magnesium