We have measured the endogenous levels of gastric and duodenal
calcitonin gene-related peptide (CGRP)-,
neurokinin A (NKA)-,
galanin-
vasoactive intestinal polypeptide (VIP)- and
neuropeptide Y (NPY)-like immunoreactivity (li) in relation to
cysteamine-induced gastric lesions and
duodenal ulcers in rats. CGRP-li but not NKA-,
galanin-, VIP- or NPY-li was decreased in gastric and duodenal samples following a single ulcerogenic dose of
cysteamine (900 mg/kg p.o.). Temporal relationships of this phenomenon showed that CGRP-li was selectively decreased (stomach 45%, duodenum 68% as compared to controls, respectively after 24 h) concomitantly to the formation of acute gastric lesions and
duodenal ulcers. Animals bearing healed
ulcers 12 days after
cysteamine, had gastroduodenal CGRP-li similar to control values. Pretreatment with the selective sensory
neurotoxin capsaicin decreased gastroduodenal CGRP-li but not NKA-,
galanin-, VIP- or NPY-li, showing that CGRP might be considered a marker of the afferent innervation of the gastroduodenal tract. The residual gastroduodenal CGRP-li levels in
capsaicin-pretreated animals were not decreased by
cysteamine administration, indicating that the effect of
cysteamine is restricted to a
peptide pool of primary afferent origin. Duodenal CGRP-li is selectively decreased by the duodenal ulcerogen
cysteamine during the acute phase of
ulcers formation and might be among the local mediators which afford protection against the ulcerogenic stimuli.