Gastric lesions induced by concentrated ethanol are associated with a decrease in gastric calcitonin gene-related peptide-like immunoreactivity in rats.

Gastric calcitonin gene-related peptide-like immunoreactivity (CGRP-li) was decreased in the gastric corpus of rats treated with 75% or 96% ethanol but not with 50% ethanol. The extent of gastric lesions was related to the increasing concentrations of ethanol (50-96%). CGRP-li decrease was evident already at 5 min after the 96% ethanol challenge, whereas a peptide recovery resulted 10 days after, concomitant with the healing of gastric lesions. Ethanol (96%) produced a significant decrease of CGRP-li in the whole thickness of the gastric corpus but not in the mucosal layers of the same area, indicating that the muscular layer of the gastric corpus is the zone involved in this phenomenon. Pretreatment with the selective sensory neurotoxin capsaicin induced a gastric CGRP-li decrease in the corpus and forestomach. Ethanol (96%) did not further decrease gastric corpus CGRP-li in capsaicin-pretreated rats. These findings suggest that 96% ethanol induced a decrease of CGRP-li deriving from a capsaicin-sensitive pool and that CGRP may play a role in gastric ulcer pathogenesis of haemorrhagic lesions induced by concentrated ethanol.