Effects of corticotropin-releasing factor on plasma motilin and somatostatin levels and gastrointestinal motility in dogs

Buéno, Lionel; Fargeas, M.J.; Gué, M.; Peeters, Theo; Bormans, Vera; Fioramonti, Jean

doi:10.1016/0016-5085(86)90690-6

Cited by 37 publications

(11 citation statements)

References 24 publications

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“…On the contrary, IP CRH reproduced colonic responses to stress; an effect that was abolished by antalarmin pretreatment, which is in line with previous studies. 29,30,59,60 Moreover, we have observed that the effects of IP CRH were not significantly different between vagotomized and sham-vagotomized animals, which further supports the notion that the intestinal effects of IP CRH were mediated by peripheral mechanisms.…”

Section: Discussionsupporting

confidence: 80%

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

et al. 2002

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When exposed to prolonged stress, rats develop gastric ulceration, enhanced colon motility with depletion of its mucin content and signs of physiological and behavioral arousal. In this model, we tested whether antidepressants (fluoxetine and bupropion), anxiolytics (diazepam and buspirone) or the novel nonpeptide corticotropin-releasing hormone (CRH) type-1 receptor (CRH-R1) antagonist, antalarmin, modify these responses. Fluoxetine, bupropion, diazepam and antalarmin all suppressed stress-induced gastric ulceration in male SpragueDawley rats exposed to four hours of plain immobilization. Antalarmin produced the most pronounced anti-ulcer effect and additionally suppressed the stress-induced colonic hypermotility, mucin depletion, autonomic hyperarousal and struggling behavior. Intraperitoneal CRH administration reproduced the intestinal but not the gastric responses to stress while vagotomy antagonized the stress-induced gastric ulceration but not the intestinal responses. We conclude that brain CRH-R1 and vagal pathways are essential for gastric ulceration to occur in response to stress and that peripheral CRH-R1 mediates colonic hypermotility and mucin depletion in this model. Nonpeptide CRH-R1 antagonists may therefore be prophylactic against stress ulcer in the critically ill and therapeutic for other pathogenetically related gastrointestinal disorders such as peptic ulcer disease and irritable bowel syndrome.

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Section: Discussionsupporting

confidence: 80%

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

et al. 2002

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“…injection of urocortin 1 or CRF reduces the amplitude of postprandial gastric contractions, inhibits jejunal motility induced by i.v. injection of motilin, and increases propulsive colonic motility in experimental animals (54,113,116,117). The motor alterations induced by CRF and urocortin 1 were reproduced in vitro in isolated stomach tissue and distal segments of the colon, which both have functional enteric neurons; this supports the idea of local peripheral action (102,105,113,118,119).…”

Section: Link Between Crf Receptors In the Brain And Stressrelated Alsupporting

confidence: 65%

Corticotropin-releasing factor receptors and stress-related alterations of gut motor function

Taché¹,

Bonaz²

2007

J. Clin. Invest.

318

285

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Over the past few decades, corticotropin-releasing factor (CRF) signaling pathways have been shown to be the main coordinators of the endocrine, behavioral, and immune responses to stress. Emerging evidence also links the activation of CRF receptors type 1 and type 2 with stress-related alterations of gut motor function. Here, we review the role of CRF receptors in both the brain and the gut as part of key mechanisms through which various stressors impact propulsive activity of the gastrointestinal system. We also examine how these mechanisms translate into the development of new approaches for irritable bowel syndrome, a multifactorial disorder for which stress has been implicated in the pathophysiology. Stress and gut motor functionA real or perceived threat to the homeostasis of mammalian organisms, originating internally or externally, triggers adaptive stress responses that affect behavior, as well as endocrine, immune, autonomic, and visceral functions (1, 2). Regarding effects in visceral functions in particular, early seminal investigations reported by Cannon and by Almy and colleagues provided clear evidence that emotional stress impacts gastric and colonic motor activity in healthy volunteers and cats (3, 4). Subsequent studies established that delayed emptying of the stomach is the most common response evoked by various acute stressors in both experimental animals and healthy human subjects (5). By contrast, in the colon, various stressors (including anxiety, dichotomous listening, fear, intermittent hand immersion in cold water, and stressful interviews) increase colonic motility in healthy subjects (5). Similarly, in rodents and dogs, stressors as diverse as open-field test, fear conditioning, loud sound, restraint, cold exposure, water avoidance, inescapable foot or tail shocks, and increased levels of cytokines induced by endotoxins stimulate propulsive colonic motor function (2, 5-7). The autonomic nervous system provides a peripheral neuronal network by which the effects of stress can be rapidly imposed on gut function. These are mediated through the sympathetic, and vagal and pelvic parasympathetic innervation of the enteric nervous system embedded into the muscular layers of the gut (8).It is becoming increasingly recognized that these interconnected brain-gut neuronal pathways activated during stress have relevance in the pathophysiology of functional bowel disorders (9-11). In particular, various stressors in the form of early life trauma, sexual abuse, maternal neglect, fear conditioning, lifethreatening events, and enteric infection have an important role in the etiology of irritable bowel syndrome (IBS), which is characterized by altered bowel movements, bloating, and visceral pain (10-13). Cyclic vomiting syndrome is another brain-gut disorder manifested by recurrent, stereotyped episodes of nausea and vomiting in the pediatric population, which is triggered by stressors related to heightened emotional state, fasting, exercise, and infection in 80% of the patients (14).A big step forward...

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“…A significantly greater incidence of phase III within 15 minutes after CRH injection than that within 15 minutes of the start of baseline suggested that this is not incidental. Exogenous CRH induces a faster rhythm of the MMC period in the proximal jejunum in dogs28 and increases post-prandial motor activities in humans,29 suggesting its stimulatory action on motility of the small intestine in certain species. Prolonged ambulatory recording of duodenal motility showed that most IBS patients show increased incidence of clustered contractions under alert conditions 18.…”

Section: Discussionmentioning

confidence: 99%

Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome

Fukudo

Nomura

Hongo

1998

Gut

343

226

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Background-Corticotropin-releasing hormone (CRH) plays a key role in modulating intestinal motility in stressed animals. Aims-To evaluate the eVect of CRH on intestinal motility in humans and to determine whether patients with irritable bowel syndrome (IBS) have an exaggerated response to CRH. Subjects-Ten IBS patients diagnosed by Rome criteria and 10 healthy controls. Methods-CRH (2 µg/kg) was intravenously administered during duodenal and colonic manometry and plasma adrenocorticotropic hormone (ACTH) was measured by radioimmunoassay. Results-CRH induced motility of the descending colon in both groups (p<0.001) and induced greater motility indexes in IBS patients than in controls (p<0.05). CRH produced duodenal phase III motor activity in 80% of the subjects and duodenal dysmotility in 40% of IBS patients. Abdominal symptoms evoked by CRH in IBS patients lasted significantly longer than those in controls (p<0.05). CRH induced significant increases in plasma ACTH levels in both groups (p<0.001) and produced significantly higher plasma ACTH levels in IBS patients than in controls (p<0.001). Conclusion-Human intestinal motility is probably modulated by exogenous CRH. The brain-gut in IBS patients may have an exaggerated response to CRH. (Gut 1998;42:845-849) Keywords: irritable bowel syndrome; corticotropin releasing factor; adrenocorticotropic hormone; colonic motility; duodenal motility Stress can alter gastrointestinal function but the mechamism of the stress induced intestinal response is still obscure.1 The detail of the brain-gut interaction is one of the most important factors of stress induced intestinal response and irritable bowel syndrome (IBS) is presumed to be a disorder of the brain-gut link. 2 We have reported that psychological stress induces colonic segmental contractions and irregular contractile activity (phase II) of the duodenal migrating motor complex (MMC) in humans and that these responses are exaggerated in IBS patients. Wrap restraint stress in rats is also reported to facilitate colonic motility and to inhibit small intestinal motility.5 6 These phenomena in rats are mimicked by intracerebroventricular [6][7][8][9] or intravenous 9 administration of corticotropin releasing hormone (CRH) and are blocked by the CRH antagonist, helical CRH 9-41 . 6-9Stress induces anxiogenic behaviour in rats and intracerebroventricular administration of CRH mimics the behavioural changes under stress. 10Furthermore, intravenous administration of CRH decreases slow wave sleep in humans. 11These findings led us to hypothesise that CRH plays a major role in the stress response of humans, both normal subjects and IBS patients. The purpose of this study was to determine whether intravenous administration of CRH aVects human gastrointestinal motility and whether CRH discriminates physiological responses in normal control subjects from those in IBS patients. Methods SUBJECTSTen normal healthy volunteers and 10 IBS patients were studied. Both groups consisted of five men and five women. Ages (controls...

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Effects of corticotropin-releasing factor on plasma motilin and somatostatin levels and gastrointestinal motility in dogs

Cited by 37 publications

References 24 publications

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

Corticotropin-releasing factor receptors and stress-related alterations of gut motor function

Impact of corticotropin-releasing hormone on gastrointestinal motility and adrenocorticotropic hormone in normal controls and patients with irritable bowel syndrome

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