Role of dihydropyridine sensitive calcium channels in glucose transport in skeletal muscle.

Glucose transport in skeletal muscle is a carrier-mediated process activated 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 mediated by muscle's voltage dependent (dihydropyridine sensitive) calcium channels. Soleus and extensor digitorum longus (EDL) muscles, isolated from rats, were incubated with the calcium channel blocker nifedipine. Basal glucose transport was decreased in both soleus and EDL by nifedipine. Treatment with nifedipine effectively blocked both insulin and contraction stimulated glucose transport in soleus. Conversely, glucose transport in EDL, although reduced, was still significantly increased over basal by both insulin and contraction, due, perhaps, to a relatively greater number of dihydropyridine receptors in EDL. These results provide evidence that contraction stimulated, as well as insulin stimulated, glucose transport is mediated in-part by dihydropyridine receptors in skeletal muscle.