Autor: | Jack A. Groot, Paul R. Saunders, Mary H. Perdue, Derrick Yates, Javier Santos, Nico P. M. Hanssen |
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Rok vydání: | 2002 |
Předmět: |
endocrine system
medicine.medical_specialty Physiology business.industry Gastroenterology Antagonist Inflammation Epithelium Pathophysiology Pathogenesis Corticotropin-releasing hormone medicine.anatomical_structure Endocrinology Internal medicine medicine Epithelial Physiology medicine.symptom business Hormone |
Zdroj: | Digestive Diseases and Sciences. 47:208-215 |
ISSN: | 0163-2116 |
DOI: | 10.1023/a:1013204612762 |
Popis: | Stress may be a contributing factor in intestinal inflammatory disease; however, the underlying mechanisms have not been elucidated. We previously reported that acute stress altered jejunal epithelial physiology. In this study, we examined both physical and psychological stress-induced functional changes in colonic mucosa. Colonic mucosal tissue from rats subjected to either 2 hr of cold-restraint stress or 1 hr of water-avoidance stress demonstrated altered ionic transport as well as significantly elevated baseline conductance (ionic permeability) and flux of horseradish peroxidase (macromolecular permeability). Intraperitoneal pretreatment with the corticotropin-releasing hormone (CRH) antagonist, a helical CRH(9-41), inhibited the stress-induced abnormalities, while exogenous intraperitoneal administration of CRH, to control rats, mimicked the stress responses and in vitro CRH increased the macromolecular permeability. These results suggest that peripheral CRH mediates stress-induced colonic pathophysiology. We speculate that a stress-induced barrier defect may allow uptake of immunogenic substances into the colonic mucosa, initiating or exacerbating intestinal inflammation. |
Databáze: | OpenAIRE |
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