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It is well known that β-adrenergic stimulation increases the intracelluar cAMP concentration through activation of adenylate cyclase (AC) and evokes marked Mg^(2+) release in the heart, liver, and kidney. The goal of this study was to investigate the effect of insulin on isoproterenol (ISO), norepinephrine (NE), forskolin (FOS), cAMP, or dimaprit (DMP) induced Mg^(2+) efflux from the perfused rat or guinea pig heart and isolated myocytes. We hypothesized that insulin would regulate Mg^(2+) efflux induced by AC activators and cAMP analogues because insulin activates phosphodiesterase (PDE) in the hearts. The Mg^(2+) content in the perfusate was significantly higher in the presence than in the absence of insulin. The addition of ISO, NE, FOS, or cAMP to perfused rat or guinea pig heart and isolated myocytes induced a marked Mg^(2+) efflux. These effluxes were inhibited by insulin. The Mg^(2+) efflux could also be induced by DMP, a histamine H2-receptor agonist, in the perfused guinea pig heart and isolatd myocytes. This effect was also inhibited by insulin. In rat heart and myocytes, the histamine H2-receptor agonist had no effect on Mg^(2+) efflux. In conclusion, these data suggest that insulin regulates Mg^(2+) homeostasis and the inhibitory effect of insulin on adrenoceptor-stimulation or AC activation induced Mg^(2+) efflux may occur through a regulation of cAMP pathway in rat and guinea pig hearts.
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