The mechanism(s) responsible for beta2-adrenergic receptor-mediated skeletal 
muscle and cardiac hypertrophy remains undefined. This study examined whether 
calcium influx through L-type calcium channels contributed to the development of 
cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy 
during an 8-day treatment with the beta2-adrenergic receptor agonist 
clenbuterol. Concurrent blockade of L-type calcium channels with nifedipine did 
not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine 
treatment alone resulted in both cardiac and soleus muscle hypertrophy (6% and 
7%, respectively), and this effect was additive to the clenbuterol-mediated 
hypertrophy in the heart and soleus muscles. The hypertrophic effects of 
nifedipine were not associated with increases in total beta-adrenergic receptor 
density, nor did nifedipine reverse clenbuterol-mediated beta-adrenergic 
receptor downregulation in either the left ventricle or soleus muscle. Both 
nifedipine and clenbuterol-induced hypertrophy increased total protein content 
of the soleus and left ventricle, with no change in protein concentration. In 
conclusion, our results support the hypothesis that beta2-adrenergic receptor 
agonist-induced muscle hypertrophy is mediated by mechanisms other than calcium 
influx through L-type calcium channels.