Characterization of a sodium-dependent magnesium efflux from magnesium-loaded rat pancreatic acinar cells.

This study investigates the mechanism of magnesium (Mg2+) transport (efflux) from the exocrine rat pancreas. Permeabilized pancreatic acini were loaded with Mg2+ by employing a high-Mg2+ (12 mM) buffer containing A23187 (6 microM). Net Mg2+ efflux was measured using the technique of atomic absorbance spectrophotometry. Incubation of preloaded acini in a buffer deficient in Mg2+ resulted in a large and time-dependent release of Mg2+ with maximal efflux occurring within 40 min. Pretreatment of loaded acini with bumetanide, SITS or ouabain had no significant effect on Mg2+ efflux. In contrast, when acini were pretreated with 10 mM dinitrophenol, 10(-4) M amiloride, 1 mM lidocaine or 1 mM quinidine there were significant (P < 0.001) decreases in net Mg2+ efflux. Replacement of extracellular sodium [Na+]o with either N-methyl-D-glucamine (NMDG), Tris or choline resulted in a significant (P < 0.001) inhibition of Mg2+ efflux. The results of this study indicate that Mg2+ transport (efflux) in pancreatic acinar cells may not be associated with the Na(+)-K(+)-ATPase, the Na(+)-K(+)-Cl- cotransporter or the anion exchanger, but with a Na(2+)-sensitive Mg2+ transport system.