ROLE OF DIHYDROPYRIDINE-SENSITIVE CALCIUM CHANNELS IN GLUCOSE-TRANSPORT IN SKELETAL-MUSCLE

Glucose transport in skeletal muscle is a carrier-mediated process act ivated by insulin and by contractile activity. Since previous evidence suggests a role for calcium influx in the activation of this process, the purpose of this study was to determine if glucose transport is me diated by muscle's voltage dependent (dihydropyridine sensitive) calci um channels. Soleus and extensor digitorum longus (EDL) muscles, isola ted from rats, were incubated with the calcium channel blocker nifedip ine. Basal glucose transport was decreased in both soleus and EDL by n ifedipine. Treatment with nifedipine effectively blocked both insulin and contraction stimulated glucose transport in soleus. Conversely, gl ucose transport in EDL, although reduced, was still significantly incr eased over basal by both insulin and contraction, due, perhaps, to a r elatively greater number of dihydropyridine receptors in EDL. These re sults provide evidence that contraction stimulated, as well as insulin stimulated, glucose transport is mediated in-part by dihydropyridine receptors in skeletal muscle.