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  • Title: Peripheral and central administration of exogenous urocortin 1 disrupts the fasted motility pattern of the small intestine in rats via the corticotrophin releasing factor receptor 2 and a cholinergic mechanism.
    Author: Yin Y, Dong L, Yin D.
    Journal: J Gastroenterol Hepatol; 2008 Jul; 23(7 Pt 2):e79-87. PubMed ID: 17944898.
    Abstract:
    BACKGROUND AND AIM: The action of the corticotrophin releasing factor (CRF) receptor on the small intestinal motility has been rarely investigated. The present study aimed to determine the effects of urocortin 1 on small intestinal motility in rats and the CRF receptor subtypes and autonomic pathways mediating the effects. METHODS: Fasted or fed rats were used to investigate the effect of intravenous or intracerebroventricular urocortin 1 on duodenum and jejunum motility. NBI-27914 and astressin(2)-B (CRF receptor 1 and 2 antagonists, respectively), atropine (an M-receptor antagonist), phentolamine (an alpha-receptor antagonist), propranolol (a beta-receptor antagonist) and N(omega)-Nitro-L-arginine (a nitric oxide synthase [NOS] inhibitor) were applied to determine the involved CRF receptor subtypes and autonomic pathways. RESULTS: In fasted rats, intravenous or intracerebroventricular injection of urocortin 1 disrupted duodenal and jejunal migrating myoelectric complex pattern, leading to an irregular spiking activity similar to the fed motility pattern. When urocortin 1 was given in the fed state, the fed motility pattern remained unchanged. In addition, urocortin 1 also inhibited small intestinal transit function. Astressin(2)-B injected intraperitoneally or intracerebroventricularly blocked urocortin 1-induced change, while NBI-27914 had no effect. The disruption of migrating myoelectric complex induced by urocortin 1 was abolished by atropine, but not affected by phentolamine, propranolol and N(omega)-Nitro-L-arginine. CONCLUSION: Intravenous or intracerebroventricular injection of urocortin 1 acts, respectively, on peripheral and central CRF receptor 2 to disrupt the intestinal migrating myoelectric complex through an M-receptor-dependent mechanism, and such change has an inhibitory effect as proved by measuring the small intestinal transit function.
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