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 rule of L-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 1 μM dexamethasone for 48 h increased L-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 L-type Ca²⁺ channel subunit α₁C. 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 L-type specific antagonist, nifedipine. In conclusion, an elevation of L-type Ca²⁺ current is involved in the process of dexamethasone-induced cardiac myocyte hypertrophy in neonatal rats.