Magnesium is one of essential minerals for all cells. In mammals it is the second most abundant intracellular cation. Magnesium shows many roles in various physiological processes. Although recent studies demonstrated that adrenergic receptor stimulation evokes marked changes in Mg^(2+) homeostasis, the regulation of Mg^(2+) by dopamine and dopamine precursors is not yet known. The purpose of this study was to identify the mobilization of Mg^(2+) by dopamine and dopamine precursors in the perfused rat livers. Mg^(2+) content was measured by atomic absorbance spectrophotometry.
Mg^(2+) efflux was increased by L-dihydroxyphenylalanine (L-dopa) or dopamine but not by L-tyrosine from rat liver. L-dopa-induced Mg^(2+) efflux was inhibited or partial inhibited by β-methyldopa and diethyldithiocarbamate (DEDC), inhibitors of catecholamines converting enzyme. But dopamine-induced Mg^(2+) efflux was not inhibited by DEDC or phenylpropargylamine, inhibitors of dopamine β-hydroxylase.
Fluphenazine, dopaminergic antagonist, inhibited dopamine-induced Mg^(2+) efflux. L-dopa-induced Mg^(2+) efflux was also inhibited or partial inhibited by fluphenazine. In addition, the Mg^(2+) efflux by L-dopa or dopamine was completely inhibited by adrenergic antagonists (propranolol and prazosine) or imipramine.
These results indicate that the Mg^(2+) efflux from rat liver could be induced by L-dopa and dopamine, and these effects can be mediated by the dopaminergic and/or adrenergic receptor stimulation.
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