Nifedipine does not impede clenbuterol-stimulated muscle hypertrophy

The mechanism(s) responsible for beta(2)-adrenergic receptor-mediated skele tal muscle and cardiac hypertrophy remains undefined. This study examined w hether calcium influx through L-type calcium channels contributed to the de velopment of cardiac and skeletal muscle (plantaris; gastrocnemius; soleus) hypertrophy during an 8-day treatment with the beta(2)-adrenergic receptor agonist clenbuterol, Concurrent blockade of L-type calcium channels with n ifedipine did not reverse the hypertrophic action of clenbuterol. Moreover, nifedipine treatment alone resulted in both cardiac and soleus muscle hype rtrophy (6% and 7%, respectively), and this effect was additive to the clen buterol-mediated hypertrophy in the heart and soleus muscles, The hypertrop hic effects of nifedipine were not associated with increases in total beta- adrenergic receptor density, nor did nifedipine reverse clenbuterol-mediate d beta-adrenergic receptor downregulation in either the left ventricle or s oleus 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 th at beta(2)-adrenergic receptor agonist-induced muscle hypertrophy is mediat ed by mechanisms other than calcium influx through L-type calcium channels.