Magnesium-calcium signalling in rat parotid acinar cells: effects of acetylcholine.

This study investigated the effects of extracellular Mg(2+) (Mg(2+)) on basal and acetylcholine (ACh)-evoked amylase secretion and intracellular free Ca(2+) (Ca(2+)) in rat parotid acinar cells. In a medium containing 1.1 mM Mg(2+), ACh evoked significant increases in amylase secretion and Ca(2+). Either low (0 mM) or elevated (5 and 10 mM) Mg(2+) attenuated ACh-evoked responses. In a nominally Ca(2+) free medium, elevated Mg(2+) attenuated basal and ACh-evoked amylase secretion and Ca(2+). In parotid acinar cells incubated with either 0, 1.1, 5 or 10 mM Mg(2+), ACh evoked a gradual decrease in Mg(2+). These results indicate that the ACh-evoked Mg(2+) efflux is an active process since Mg(2+) has to move against its gradient. Either lidocaine, amiloride, N-methyl-D: -glucamine, quinidine, dinitrophenol or bumetanide can elevate Mg(2+) above basal level. In the presence of these membrane transport inhibitors, ACh still evoked a decrease in Mg(2+) but the response was less pronounced with either Na(+) removal or in the presence of either amiloride or quinidine. These results indicate marked interactions between Ca(2+) and Mg(2+) signalling in parotid acinar cells and that ACh-evoked Mg(2+) transport was not dependent upon Na(+).