Central nervous system effects of corticotropin-releasing factor on gastrointestinal transit in the rat

Lenz, H. J.; Burlage, Michael; Raedler, Andreas; Greten, H.

doi:10.1016/0016-5085(88)90229-6

Cited by 139 publications

(128 citation statements)

References 18 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: 81%

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: 81%

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

et al. 2002

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“…h/rCRF and rUcn, which display high affinity for CRF 1 (30,32), administered intraperitoneally or intravenously stimulate colonic motor function in rats. This was shown by the induction of clustered spike burst activity in the cecum and proximal colon, acceleration of large intestinal transit (as monitored by labeled chromium distribution from the cecum to the colon), defecation (5,6,15,18,39), and shortening of distal colonic transit (present study). In addition, the selective CRF 1 antagonist CP-154,526 prevented the intravenous h/rCRF-induced decrease in colonic bead expulsion time whereas the selective CRF 2 antagonist astressin 2 -B, injected subcutaneously at a dose that prevented the gastric response, did not.…”

Section: Discussionsupporting

confidence: 56%

Human urocortin II, a new CRF-related peptide, displays selective CRF₂-mediated action on gastric transit in rats

Million

Maillot

Saunders

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

100

129

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Human urocortin (hUcn) II is a new member of the corticotropin-releasing factor (CRF) family that selectively binds to the CRF2 receptor. We investigated the CRF receptors involved in mediating the effects of hUcn II and human/rat CRF (h/rCRF) on gut transit. Gastric emptying, 4 h after a solid meal, and distal colonic transit (bead expulsion time) were monitored simultaneously in conscious rats. CRF antagonists were given subcutaneously 30 min before intravenous injection of peptides or partial restraint (for 90 min). hUcn II (3 or 10 g/kg iv) inhibited gastric emptying (by 45% and 55%, respectively) and did not influence distal colonic transit. The CRF2 peptide antagonist astressin2-B blocked hUcn II action. h/rCRF, rat Ucn, and restraint delayed gastric emptying while accelerating distal colonic transit. The gastric response to intravenous h/rCRF and restraint was blocked by the CRF2 antagonist but not by the CRF1 antagonist CP-154,526, whereas the colonic response was blocked only by CP-154,526. None of the CRF antagonists influenced postprandial gut transit. These data show that intravenous h/rCRF and restraint stress-induced delayed gastric emptying involve CRF2 whereas stimulation of distal colonic transit involves CRF1. The distinct profile of hUcn II, only on gastric transit, is linked to its CRF2 selectivity. partial restraint; gastric emptying; distal colonic transit; CP-154,526; astressin2-B

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“…NPY injected into the rat lateral brain ventricle at a similar dose-range was previously shown to prevent intracerebroventricular injection of CRF-and psychological stress-induced stimulation of colonic motor activity (Jimenez & Bueno, 1990;Junien et al, 1991). Increased colonic transit in response to stress exposure involves endogenous release of CRF in the brain (Williams et al, 1987;Lenz et al, 1988a;Gue et al, 1991;Monnikes et al, 1992). Taken together these data indicate that NPY can antagonize the alterations of gastrointestinal secretory and motor function induced by exogenous or endogenous CRF.…”

Section: Discussionsupporting

confidence: 57%

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

Gué¹,

Yoneda

Mönnikes

et al. 1992

British J Pharmacology

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4 CRF (3 jig) microinjected into the hypothalamic paraventricular nucleus (PVN) and the lateral hypothalamus (LH) inhibited pentagastrin-stimulated gastric acid secretion by 61% and 51%; NPY (0.03 gg) or JO 1784 (0.03 gig) microinjected into the PVN had no effect by themselves but blocked CRF antisecretory action. Microinjection into the LH had no effect. 5 In conclusion, NPY and JO 1784 (a sigma ligand) interacts with CRF in the PVN to block CRF-induced inhibition of pentagastrin-stimulated gastric acid secretion. The central action of JO 1784 and NPY is specific to CRF and may involve sigma binding sites.

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Central nervous system effects of corticotropin-releasing factor on gastrointestinal transit in the rat

Cited by 139 publications

References 18 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

Human urocortin II, a new CRF-related peptide, displays selective CRF₂-mediated action on gastric transit in rats

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

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Central nervous system effects of corticotropin-releasing factor on gastrointestinal transit in the rat

Cited by 139 publications

References 18 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

Human urocortin II, a new CRF-related peptide, displays selective CRF2-mediated action on gastric transit in rats

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

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Human urocortin II, a new CRF-related peptide, displays selective CRF₂-mediated action on gastric transit in rats