Effect of treatment with nifedipine, an L-type calcium channel blocker, on muscular atrophy induced by hindlimb immobilization.

Abstract

The purpose of this study was to investigate whether the prevention of calcium influx through L-type calcium channels contributed to the attenuation of muscular atrophy induced by hindlimb immobilization (HI) in a shortened position. Mice were divided into four groups (8 mice/group): control; nifedipine; HI; and HI with nifedipine. Mice received nifedipine at a dose of 5 mg/kg one day before and during the 8 days of HI. Quantitative alterations in the amount of myosin heavy chain (MyHC) and actin proteins in the soleus muscle were analyzed using SDS-PAGE. The weight of the soleus muscle decreased significantly by 40.8% (P<0.05) and 27.0% (P<0.05) after the hindlimb immobilization in the HI and HI with nifedipine groups, respectively, when compared to that of the control or nifedipine groups. Treatment with nifedipine alone appeared to have no effect on muscle mass or the amount of myofibrillar proteins. The level of MyHC proteins decreased significantly by 25.1% (P<0.001) and 17.4% (P<0.001) in the HI and HI with nifedipine groups, respectively. The level of MyHC protein in the HI with nifedipine group was significantly greater than that of the HI group (P<0.05), although there were no significant differences in the amount of actin protein. These findings suggest that nifedipine treatment may have a beneficial effect on muscular atrophy.