Duchenne muscular dystrophy (DMD) is a common genetic disorder characterized by a severe muscle wasting caused by the absence of dystrophin. In mdx muscle fibers, we have shown that basal ATP release is increased and that high extracellular ATP is a pro‐apoptotic stimuli. We also have shown that Dihydropyridine receptors (DHPR) are needed for ATP release through pannexin‐1(Pnx1) channels. The aim of this work was to study the potential therapeutic effect of DHPR blockage by nifedipine in DMD. We used muscle fibers isolated from six‐week‐old normal and mdx mice that were treated with daily intraperitoneal injections of 1mg/Kg nifedipine for 1‐week. We studied differences in the interaction between DHPR and Pnx1by proximity ligation assay. In mdx fibers there was an increase in the number and volume of positive particles but not in the intensity of the positive reaction when compared to normal fibers. After the treatment with nifedipine, both number and volume of the positive reaction particles was normalized. This result correlates well with a decrease in both ATP release and intracellular resting Ca2+ concentration in mdx fibers after the treatment. Moreover, ATP signaling was no longer a pro‐apoptotic stimuli. Finally, nifedipine treatment increased muscle strength assessed by both the inverted grip‐hanging and forced swimming test. These data suggest that dihydropyridines can be used as a therapeutical tool to reduce muscle damage observed in dystrophic muscles. Grant Funding Source: Fondecyt 1110467, ACT1111, AFM14562, AT‐24110211