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

Abstract

This study investigated the effects of extracellular Mg(2+) ([Mg(2+)](o)) on basal and acetylcholine (ACh)-evoked amylase secretion and intracellular free Ca(2+) ([Ca(2+)](i)) in rat parotid acinar cells. In a medium containing 1.1 mM [Mg(2+)](o), ACh evoked significant increases in amylase secretion and [Ca(2+)](i). Either low (0 mM) or elevated (5 and 10 mM) [Mg(2+)](o) attenuated ACh-evoked responses. In a nominally Ca(2+) free medium, elevated [Mg(2+)](o) attenuated basal and ACh-evoked amylase secretion and [Ca(2+)](i). In parotid acinar cells incubated with either 0, 1.1, 5 or 10 mM [Mg(2+)](o), ACh evoked a gradual decrease in [Mg(2+)](i). 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+)](i) above basal level. In the presence of these membrane transport inhibitors, ACh still evoked a decrease in [Mg(2+)](i) but the response was less pronounced with either [Na(+)](o) 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(+)](o).

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