Role of Ca2+ in corticosterone-induced muscle growth retardation

The increased plasma glucocorticoid concentration in stressful conditions stimulates muscle protein degradation, and results in growth retardation in animals. However, the mechanism is still to be clarified. The present study was undertaken to examine the participation of Ca²⁺ in the glucocorticoid action, using nifedipine (NIF), a Ca²⁺ channel antagonist. The effects of NIF on growth, differentiation, and protein degradation were examined in glucocorticoid-treated primary cultured chick muscle cells. Muscle cell growth and cell differentiation were assessed by protein content and creatine kinase (CK) activity, respectively, and the rate of myofiblillar protein degradation was estimated by the release of N ^τ-methylhistidine (MeHis). Creatine kinase activity was increased by corticosterone (CTC) and this effect was minimized by NIF. Protein content was decreased by CTC and normalized by NIF. N ^τ-methylhistidine release was significantly increased by CTC and tended to be minimized by NIF. The present results indicate that CTC increases skeletal muscle proteolysis followed by muscle growth retardation partially because of enhanced Ca²⁺ influx through the NIF-sensitive Ca²⁺ channel. Enhanced muscle differentiation by CTC is mediated also by the NIF-sensitive Ca²⁺ channel.