Korean J Physiol Pharmacol.
1997 Dec;1(6):717-730.
Regulation of Mg2+ release in guinea pig heart and isolated ventricular
myocytes by alpha1-adrenergic stimulation
- Affiliations
-
- 1Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University, Chonju, Chonbuk 561-756, South Korea.
Abstract
-
Mg2+ 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 Mg2+ in mammalian
cells is not fully understood. More recently, however, the mechanism of
Mg2+ mobilization by hormonal stimulation has been investigated in
hearts and in myocytes. In this work we have investigated the
regulation mechanism responsible for the Mg2+ mobilization induced by
alpha1-adrenoceptor stimulation in perfused guinea pig hearts or
isolated myocytes. The Mg2+ content of the perfusate or the supernatant
was measured by atomic absorbance spectrophotometry. The elimination of
Mg2+ in the medium increased the force of contraction of right
ventricular papillary muscles. Phenylephrine also enhanced the force of
contraction in the presence of Mg2+/-free medium. alpha1-Agonists such
as phenylephrine were found to induce Mg2+ efflux in both perfused
hearts or myocytes. This was blocked by prazosin, a alpha1-adrenoceptor
antagonist. Mg2+ efflux by phenylephrine was amplified by Na+ channel
blockers, an increase in extracellular Ca2+ or a decrease in
extracellular Na+. By contrast, the Mg2+ influx was induced by
verapamil, nifedipine, ryanodine, lidocaine or tetrodotoxin in perfused
hearts, but not in myocytes. W7, a Ca2+/calmodulin antagonist,
completely blocked the phenylephrine-, A23187-, veratridine-,
Ca2+/-induced Mg2+ efflux in perfused hearts or isolated myocytes. In
addition, Mg2+ efflux was induced by W7 in myocytes but not in perfused
heart. In conclusion, An increase in Mg2+ efflux by alpha1-adrenoceptor
stimulation in hearts can be through IP3 and Ca2+/-calmodulin dependent
mechanism.