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Regulation by extracellular Na + of cytosolic Mg 2+ concentration in Mg 2+ ‐loaded rat sublingual acini
Author(s) -
Zhang Guo H.,
Melvin James E.
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00869-b
Subject(s) - extracellular , chemistry , cytosol , antiporter , efflux , vanadate , carbachol , ion transporter , depolarization , biophysics , muscarinic acetylcholine receptor , endocrinology , medicine , biochemistry , membrane , biology , enzyme , receptor
The regulation of cytosolic free Mg 2+ concentration ([Mg 2+ ] 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 Mg 2+ elevated the [Mg 2+ ] i from 0.35 ± 0.01 mM to 0.66 ± 0.01 mM. Removal of extracellular Mg 2+ resulted in a significantly faster [Mg 2+ ] i decrease in Mg 2+ ‐loaded rcini than in unloaded acini. Membrane depolarization with high extracellular [K + ] and inhibition of P‐type ATPases by vanadate did not alter the [Mg 2+ ] i decrease, indicating that the Mg 2+ efflux mechanism is not electrogenic. Na + ‐free medium inhibited 80% of the [Mg 2+ ] i decrease suggesting that a Na + ‐dependent Mg 2+ efflux pathway mediates the [Mg 2+ ] i decrease. Accordingly, the Na + ‐dependent antiport inhibitor quinidine reduced > 80% of the [Mg 2+ ] i decrease, suggesting that the Na + ‐dependent Mg + efflux was also partly driven by K + . The [Mg + ] i system. Mg 2+ efflux was also partly driven by K + . The [Mg 2+ ] i decrease 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 Mg 2+ efflux and that muscarinic stimulation may regulate Mg 2+ extrusion.