Korean Journal of Veterinary Research 2001;41(3):319-325.
The regulation of Mg2+ efflux by melatonin in perfused guinea pig hearts
Hyo-jin Chang, Ji-hea Youk, Jin-shang Kim
Bio-Safety Research Institute, Chonbuk National University
관류 기니픽 심장에서 melatonin에 의한 Mg2+ 유리 조절
장효진, 육지혜, 김진상
전북대학교 생체안전성연구소
Several recent studies demonstrate that cAMP accumulation evokes marked changes in magnesium ($Mg^{2+}$) homeostasis. The goal of this study was to investigate the effect of melatonin, the principal hormone of the vertebral pineal gland, on $Mg^{2+}$ regulation in perfused guinea pig hearts. We hypothesized that melationin would regulate $Mg^{2+}$ efflux induced by adrenergic drugs and cAMP analogues because melatonin inhibites adneylate cyclase (AC) and phospholipase C(PLC) in the hearts. The $Mg^{2+}$ content in the perfusate was significantly higher in the presence than in the absence of melatonin. The addition of forskolin, isoproterenol or dimaprit to perfused hearts induced a marked $Mg^{2+}$ efflux. These effluxes were not inhibited by melatonin. The $Mg^{2+}$ efflux could also be induced by phenylephrine, a ${alpha}_1$-adrenoceptor agonist. This phenylephrine-induced $Mg^{2+}$ efflux was inhibited by melatonin. In addition, the phenylephrine-induced $Mg^{2+}$ efflux was potentiated by PMA, a protein kinase C(PKC) activator. This $Mg^{2+}$ efflux was inhibited by melatonin. In conclusion, these data suggest that melatonin regulates $Mg^{2+}$ homeostasis and the inhibitory effect of melatonin on ${alpha}_1$-adrenoceptor-stimulated $Mg^{2+}$ efflux may occur through an inhibition of PLC pathway in perfused guinea pig hearts.
Key Words: magnesium, melatonin, ${alpha}1$ - adrenoceptor, heart

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