Regulation by extracellular Na+ of cytosolic Mg2+ concentration in Mg(2+)-loaded rat sublingual acini.

The regulation of cytosolic free Mg2+ concentration ([Mg2+]i) in Mg(2+)-loaded rat sublingual mucous acini was examined using the Mg(2+)-sensitive fluorescent indicator mag-fura-2. Loading sublingual acini with 5 mM Mg2+ elevated the [Mg2+]i from 0.35 +/- 0.01 mM to 0.66 +/- 0.01 mM. Removal of extracellular Mg2+ resulted in a significantly faster [Mg2+]i decrease in Mg(2+)-loaded acini than in unloaded acini. Membrane depolarization with high extracellular [K+] and inhibition of P-type ATPases by vanadate did not alter the [Mg2+]i decrease, indicating that the Mg2+ efflux mechanism is not electrogenic. Na(+)-free medium inhibited 80% of the [Mg2+]i decrease suggesting that a Na(+)-dependent Mg2+ efflux pathway mediates the [Mg2+]i decrease. Accordingly, the Na(+)-dependent antiport inhibitor quinidine reduced > 80% of the [Mg2+]i decrease, suggesting that the Na(+)-dependent Mg2+ efflux is mediated by the Na+/Mg2+ antiport system. Mg2+ efflux was also partly driven by K+. The [Mg2+]i decreased was significantly inhibited by carbachol, a muscarinic agonist, but not by cAMP. These results indicate that in sublingual acinar cells a Na(+)-dependent pathway mediates Mg2+ efflux and that muscarinic stimulation may regulate Mg2+ extrusion.