Effects of dopaminergic receptor stimulation on Mg2+ regulation in the rat heart and isolated ventricular myocytes

Kang, H.S.; Kim, J.S.; Kim, J.S. . College of Veterinary Medicine

Effects of dopaminergic receptor stimulation on Mg2+ regulation in the rat heart and isolated ventricular myocytes

1999

Kang, H.S. | Kim, J.S. | Kim, J.S. (Chonbuk National University, Chonju (Korea Republic). College of Veterinary Medicine)

Magnesium(Mg2+) is one of the most abundant intracellular divalent cation. Although recent studies demonstrate that adrenergic receptor stimulation evokes marked changes in Mg2+ homeostasis, the regulation of Mg2+ by dopaminergic receptor stimulation is not yet known. In this work, we uwed dopaminergic agents to identify which type(s) of receptors were involved inthe mobilization of Mg2+ by dopaminergic receptor stimulation in the perfused rat gearts, isolated myocytes and circulating blood. The mg2+ content was measured by atomic absorbance spedtrophotometry. Dopamine(DA), apomorphine(APO) and pergolide stimulated Mg2+ efflux in the perfused rat hearts and these effects were inhibited by haloperidol or fluphenazine, nonselective dopaminergic antagonists. SKF38393, a selective doparminergic agonist, increased Mg2+ efflux from the perfused hearts in dose dependant manners and SKF38393-induced Mg2+ efflux was potentiated in the presence of sulpiride or eticlopride, D2-selective antagonist, from the perfused hearts. This increase of Mg2+ efflux was blocked by haloperidol or imipramine. DA or pergolide increased in circulating Mg2+ from blood. By contrast, PPHT stimulated Mg2+ influx(a decrease in efflux) from the perfused hearts and circulating blood. PPHT-induced Mg2+ influx was blocked by fluphenazine in the perfused hearts. DA-stimulated Mg2+ efflux was inhibited by dopaminergic antagoinst in the isolated myocytes. In conclusion, the flux of Mg2+ is modulated by DA receptor activation in the rat hearts. The efflux of Mg2+ can be increased by D1-receptor stimulation and decreased by D2-receptor stimulation, respectively.

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