Impaired nitrergic relaxations in the gastric fundus of dystrophic (mdx) mice

Relaxant responses to electrical field stimulation (EFS) were investigated in the gastric longitudinal fundus strips from young normal and mdx dystrophic mice, an animal model of Duchenne muscular dystrophy. In carbachol (CCh) precontracted strips from normal mice, EFS elicited brisk relaxant responses that, depending on stimulation frequency, could be followed by a sustained relaxation. In strips from mdx mice the brisk relaxation was impaired. Smooth muscle responses to direct stimulating agents did not differ in amplitude between the two groups of animals. In strips from both normal and mdx mice, N(G)-nitro-L-arginine (L-NNA) abolished the brisk phase of relaxation, without affecting the sustained response. alpha-chymotrypsin abolished, in both preparations, the sustained relaxant response to EFS as well as relaxation to vasoactive intestinal polypeptide. Results suggest that, in strips from mdx mice, a defective production/release of the neurotransmitter responsible for the brisk relaxation, likely nitric oxide, occurs.