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기니픽에서 Magnesium의 혈관 이완과 혈압 하강 효과
김정곤,강형섭,김진상 한국수의공중보건학회 2003 예방수의학회지 Vol.27 No.2
The present study evaluated the effects of various agents on magnesium sulfate (Mg^(2+))-induced relaxation in aorta and blood pressure lowering in anesthetized guinea pigs. Mg^(2+) inhibited phenylephrine (PE)- or 40 mM KC1-induced sustained contraction of endothelium-intact (+E) guinea pig aortic rings in concentration-dependent manner. In preparations preconstricted with PE or KC1, Mg^(2+)-induced concentration-dependent relaxations. In preparations preconstricted with PE or KCl, Mg^(2+)-induced relaxations were not affected by the removal of endothelium (-E) and by the pretreatment of aortic rings with NO synthase (NOS) inhibitors (L-NAME and LNNA), guanylate cyclase inhibitors (methylene blue and ODQ, adenylate cyclase inhibitor (MDL), K^(+) channel blockers (glibenclamide and tetrabutylammonium), nifedipine or ryanodine. However, Mg^(2+)-induced relaxations were inhibited by Na^(+)-Mg^(2+) exchange inhibitor (imipramine) or removal (or attenuation) of extracellular Ca^(2+) in +E aortic rings. PE-induced contraction was not inhibited by nifedipine. In addition, Mg^(2+)-induced relaxations were inhibited by phospholipase C inhibitor (NCDC) or inositol monophosphatase inhibitor (lithium), but not by protein kinase C inhibitor (staurosporine). In vi패 infusion of Mg^(2+), directly into the femoral veins of guinea pigs, elicited sustained decrease in arterial blood pressure. The Mg^(2+)-lowered blood pressure was attenuated by intravenous administration of imipramine or lithium, but not by methylene blue, indomethacin, tetrabutylammonium nifedipine, LNNA, L-NAME or saponin (as an endothelium removal agent). These results suggest that endothelium independent vasorelaxant effect of Mg^(2+) on aortic ring appear to play important roles on the antihypertensive action in guinea pig, most likely via the inhibitory action of Mg^(2+) on the intracellular C^(2+) involve in PLC-IP pathway and influx (through the Na^(+)-Mg^(2+) exchanger) into the cell in guinea pig aorta.
관류 심장과 심장 세포에서 Insulin에 의한 Mg^(2+) 유리 조절
정창우,강형섭,김진상 한국수의공중보건학회 2002 예방수의학회지 Vol.26 No.3
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.