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- W2399692321 abstract "is the fourth most abundant cation in cellular organisms. Although the biological chemistry and the physiological roles of the magnesium ion were well known, the regulation of intracellular in mammalian cells is not fully understood. More recently, however, the mechanism of mobilization by hormonal stimulation has been investigated in hearts and in myocytes. In this work we have investigated the regulation mechanism responsible for the mobilization induced by stimulation in perfused guinea pig hearts or isolated myocytes. The content of the perfusate or the supernatant was measured by atomic absorbance spectrophotometry. The elimination of in the medium increased the force of contraction of right ventricular papillary muscles. Phenylephrine also enhanced the force of contraction in the presence of -free medium. such as phenylephrine were found to induce efflux in both perfused hearts or myocytes. This was blocked by prazosin, a antagonist. efflux by phenylephrine was amplified by channel blockers, an increase in extracellular or a decrease in extracellular . By contrast, the influx was induced by verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused hearts, but not in myocytes. , a antagonist, completely blocked the pheylephrine-, A23187-, veratridine-, efflux in perfused hearts or isolated myocytes. In addition, efflux was induced by in myocytes but not in perfused heart. In conclusion, An increase in efflux by stimulation in hearts can be through and dependent mechanism." @default.
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- W2399692321 date "1997-01-01" @default.
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- W2399692321 title "Regulation of $Mg^{2+}$ Release in Guinea Pig Heart and Isolated Ventricular Myocytes by ${alpha}_1-Adrenergic$ Stimulation" @default.
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