Magnesium (Mg²⁺) is an abundant divalent cation in cells and it plays a vital role in the regulation of a number of biochemical and physiological processes including ion transport and digestive enzyme secretion (Yago et al. 2000). Moreover, a perturbation of extracellular Mg²⁺ ([Mg²⁺]_o) has profound effects on secretagogue-evoked calcium (Ca²⁺) mobilisation and on amylase secretion in the pancreas (Francis et al. 1990) and parotid salivary glands (Yago et al. 2002). This study investigated the effects of acetylcholine (ACh), several membrane transport inhibitors and substituting [Na⁺]_o with N-Methyl-D-glutamine (NMDG) on cytosolic Mg²⁺ concentration ([Mg²⁺]_i) in magfura-2-loaded single rat parotid acinar cells using microspectrofluorimetric techniques to measure [Mg²⁺]_i (Mooren et al. 2001). The cells used came from humanely killed rats.

Basal [Mg²⁺]_i in zero mM, 1.1 mM, 5 mM and 10 mM [Mg²⁺]_o was (mean ± S.E.M.) 0.263 ± 0.0116; 0.304 ± 0.0101; 0.425 ± 0.0317 and 0.0495 ± 0.0161 ratio units (n = 25-30 cells taken from 10-15 animals ). Stimulation of magfura-2-loaded parotid acinar cells with 10^-5 M ACh resulted in a marked decrease in the [Mg²⁺]_i. Typically, [Mg²⁺]_i decreased from its respective basal to (mean ± S.E.M.) 0.241 ± 0.047; 0.277 ± 0.009; 0.403 ± 0.03 and 0.453 ± 0.011 ratio units in zero mM, 1.1 mM, 5 mM and 10 mM [Mg²⁺]_o, respectively. Superfusion of parotid acinar cells with different (zero mM, 1.1 mM, 5 mM and 10 mM) [Mg²⁺]_o resulted in a gradual increase in [Mg²⁺]_i. In the continuous presence of 10 mM [|Mg²⁺]_o ACh evoked a rapid decrease in [Mg²⁺]_i. Superfusion of parotid acinar cells with either 10^-3 M lidocaine, NMDG instead of [Na⁺]_o, 10^-3 M amiloride, 10^-3 M quinidine, 10-4 dinitrophenol or 10^-3 M bumetanide resulted in a significant (Student’s t test, (P < 0.05)) elevation in [Mg²⁺]_i compared to basal [Mg²⁺]_i. Typically, [Mg²⁺]_i was increased from a basal of 0.304 ± 0.010 ratio units to 0.402 ± 0.022; 0.509 ± 0.004; 0.563 ± 0.033; 0.662 ± 0.015; 0.778 ± 0.073 and 0.931 ± 0.058 ratio units (n = 8-12) for lidocaine, amiloride, NMDG, quinidine, dinitrophenol and bumetanide, respectively. In the continuous presence of each of these membrane transport inhibitors, ACh (10^-5 M) elicited a marked decrease in [Mg²⁺]_i compared to the respective control in the presence of each inhibitor. The decrease in [Mg²⁺]_i was much larger in the presence of bumetanide compared to the responses obtained in the presence of the other transport inhibitors or Na⁺ substitution.

The results indicate that the ACh-evoked decrease in [Mg²⁺]_i in parotid acinar cells is insensitive to sodium removal and to a number of membrane transport inhibitors which themselves can increase [Mg²⁺]_i.