title: Brain ACTH prevents stress gastric lesions in rats.
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 ACTH1-39 dose-dependently (0.1-10 micrograms) inhibited stress gastric lesion formation. Studies with smaller molecular weight forms of ACTH (in a dose equimolar to 10 micrograms of ACTH1-39) revealed that ACTH1-13 and ACTH1-10 were also protective. The ACTH fragments ACTH5-10, ACTH34-39 and ACTH1-17 were without effect. Immunoneutralization of endogenous brain ACTH1-39 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 beta-endorphin suggest that specific brain pro-opiomelanocortin gene products modulate gastric mucosal integrity in response to stress.
authors.affiliation: Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.
authors.forename: D E
authors.initials: DE
authors.lastname: Hernandez
authors.forename: P
authors.initials: P
authors.lastname: Morin
authors.forename: A B
authors.initials: AB
authors.lastname: Salaiz
authors.forename: M A
authors.initials: MA
authors.lastname: Moreira
authors.forename: L
authors.initials: L
authors.lastname: Jennes
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000502:physiology*; D000818:Animals; D001923:Brain Chemistry / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D007276:Injections, Intraventricular; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000503:physiopathology*; D013312:Stress, Physiological / Q000503:physiopathology*
chemical_list: D010446:Peptide Fragments; D000324:Adrenocorticotropic Hormone