Abstract
This study evaluated the effect of ACTH and several ACTH fragments on the development of gastric glandular lesions induced by cold-restraint stress in rats. Intracerebroventricular administration of ACTH 1–39 dose-dependently (0.1–10 μg) inhibited stress gastric lesion formation. Studies with smaller molecular weight forms of ACTH (in a dose equimolar to 10 μg of ACTH 1–39) revealed that ACTH 1–13 and ACTH 1–10 were also protective. The ACTH fragments ACTH 5–10, ACTH 34–39 and ACTH 1–17 were without effect. Immunoneutralization of endogenous brain ACTH 1–39 significantly increased stress gastric lesion severity. Antisera raised against synthetic somatostatin, gonadotropin-releasing hormone, and L-enkephalin were ineffective. These results with ACTH coupled with our previous demonstration of a protective effect of β-endorphin suggest that specific brain pro-opiomelanocortin gene products modulate gastric mucosal integrity in response to stress. Brain ACTH ACTH fragments Stress ulcers ACTH antiserum Male rats
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