Dexamethasone-induced Hypertrophy in Rat Neonatal Cardiac Myocytes Involves an Elevated L-type Ca2+Current

The mechanism responsible for dexamethasone-induced hypertrophy in infants has not been defined. In this study, we have investigated the role of -type Ca2+currents in the development of dexamethasone-induced hypertrophy in rat neonatal cardiac myocytes. Using cytoplasmic membrane capacitance measurements, we have shown that the size of the cells treated with dexamethasone were larger than those of the control cells. In addition, treating the cells with 1μmdexamethasone for 48 h increased -type Ca2+current density significantly, without affecting the voltage-dependent activation and steady state inactivation of the current. The increase in current density was associated with an elevation of the mRNA transcript encoding the -type Ca2+channel subunitα1C. Dexamethasone treatment also resulted in an increase in the peak amplitude of the intracellular Ca2+transient measured by fura-2/epifluorescence. Finally, we have demonstrated that the hypertrophic effect of dexamethasone, characterized by the ratio of protein content per cell, was blocked by the -type specific antagonist, nifedipine. In conclusion, an elevation of -type Ca2+current is involved in the process of dexamethasone-induced cardiac myocyte hypertrophy in neonatal rats.