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Nifedipine does not impede clenbuterol-stimulated muscle hypertrophy
R J Murphy1, L Béliveau, P F Gardiner
1Département de Kinésiologie, Université de Montréal, Montreal, Canada H3C 3J7.
Abstract:
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.
Insights
Beta2-adrenergic receptor agonist-induced muscle growth is not dependent on L-type calcium channels. Blocking these channels with nifedipine did not inhibit clenbuterol
Area of Science:
- Muscle physiology
- Pharmacology
Background:
- Beta2-adrenergic receptor agonists like clenbuterol promote muscle hypertrophy.
- The precise mechanisms driving this hypertrophy are not fully understood.
Purpose of the Study:
- To investigate the role of L-type calcium channels in beta2-adrenergic receptor-mediated muscle hypertrophy.
- To determine if blocking L-type calcium channels affects clenbuterol-induced cardiac and skeletal muscle growth.
Main Methods:
- Administered clenbuterol to induce muscle hypertrophy.
- Used nifedipine to block L-type calcium channels concurrently or alone.
- Measured changes in cardiac and skeletal muscle mass and protein content.
Main Results:
- Nifedipine did not prevent clenbuterol-induced hypertrophy in cardiac and skeletal muscles.
- Nifedipine alone caused significant cardiac and soleus muscle hypertrophy.
- Nifedipine-induced hypertrophy was additive to clenbuterol effects and not linked to beta-adrenergic receptor density changes.
Conclusions:
- Calcium influx via L-type calcium channels is not the primary mechanism for beta2-adrenergic receptor agonist-induced muscle hypertrophy.
- L-type calcium channel blockade alone can induce muscle hypertrophy, suggesting alternative pathways involved in muscle growth regulation.