Involvement of interleukin‐1, prostaglandins and mast cells in rectal distension‐induced colonic water secretion in rats

Eutamène, Hélène; Théodorou, Vassilia; Vergnolle, Nathalie; Coméra, Christine; Fioramonti, Jean; Buéno, Lionel

doi:10.1111/j.1469-7793.1998.245bx.x

Cited by 12 publications

(15 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data indicate that both acute and chronic PRS similarly increase both mast cell histamine synthesis and sensitivity to SP, as shown by an increase in histamine release after SP stimulation in colonic samples of stressed rats. However, the number of mast cells was also unchanged after C‐PRS, as has previously been shown for A‐PRS 30 . This result is consistent with a previous study, 30 and suggests a modulatory role of stress on mast cell mediators, independent of stress stimuli chronicity, resulting in enhanced levels of histamine content.…”

Section: Discussionsupporting

confidence: 91%

Acute and chronic stress differently affect visceral sensitivity to rectal distension in female rats

Bradesi¹,

Eutamène

Garcia‐Villar³

et al. 2002

Neurogastroenterology Motil

Self Cite

View full text Add to dashboard Cite

Stressful life events are frequently associated with outward signs of irritable bowel syndrome (IBS). Increasing evidence suggests that acute and chronic stress stimuli implicate different physiological mechanisms and neuroendocrine responses. Therefore, we investigated the influence of acute and chronic stress on visceral nociception in female rats and the involvement of colonic mast cells in this effect. The effect of acute and chronic partial restraint stress (PRS) on visceral sensitivity to rectal distension (RD) was assessed by abdominal muscle electromyography. Colonic mast cell activation was determined by measuring histamine release after in vitro stimulation with substance P (SP) in colonic samples from rats experiencing RD vs. controls. Acute PRS significantly enhanced abdominal response to RD compared with sham PRS for all volumes of distension. In contrast, chronic PRS induced a hyperalgesic response for the highest volumes of distension (0.8 and 1.2 mL), but did not affect the number of abdominal contractions for the lowest volume (0.4 mL) compared with controls. Both acute and chronic PRS increased in vitro SP-induced histamine release without affecting mast cell numbers. RD induced similar in vitro histamine release from colonic samples from both acute and chronic PRS rats; this release, however, was significantly higher than that measured in sham-PRS rats. Acute and chronic PRS differently influence visceral sensitivity in response to RD in female rats. This difference, however, cannot be attributed to a different effect of either stress paradigm on mast cell histamine release.

show abstract

Section: Discussionsupporting

confidence: 91%

Acute and chronic stress differently affect visceral sensitivity to rectal distension in female rats

Bradesi¹,

Eutamène

Garcia‐Villar³

et al. 2002

Neurogastroenterology Motil

Self Cite

View full text Add to dashboard Cite

show abstract

“…Further this group showed that peripheral administration of a mast cell stabilizer suppressed the stress-and CRF-induced hypersensitivity to rectal distension. In addition, they found that the level of histamine released from the intestines of stressed rats was significantly increased in vitro, whereas the number of mucosal mast cells was unchanged compared to the control group [85,86]. These data suggest that intestinal mast cells become more sensitive to a mast cell degranulator after stress and reinforce the hypothesis for a role of mast cells in stressinduced visceral hypersensitivity.…”

Section: Mechanisms Of Stress Effects On Gi Sensitivity In Experimentsupporting

confidence: 71%

“…These data suggest that intestinal mast cells become more sensitive to a mast cell degranulator after stress and reinforce the hypothesis for a role of mast cells in stressinduced visceral hypersensitivity. The sensitized mast cells may be responsible for the visceral hypersensitivity in response to stress through a higher synthesis and later on release of histamine and/or other mast cell mediators [85][86][87]. Despite the fact that the number of mast cells in stressed rats was unchanged compared to the control group -which is contrary to studies in IBS patients who have been shown to present more mast cells than healthy controls [88] -this idea is in agreement with neuroanatomical studies and data obtained in humans showing a close proximity of mucosal mast cells with the enteric nervous system [77].…”

Section: Mechanisms Of Stress Effects On Gi Sensitivity In Experimentmentioning

confidence: 99%

Role of Stress in Functional Gastrointestinal Disorders

Mönnikes

Tebbe²,

Hildebrandt³

et al. 2001

Dig Dis

233

View full text Add to dashboard Cite

Psychological stress is widely believed to play a major role in functional gastrointestinal (GI) disorders, especially irritable bowel syndrome (IBS), by precipitating exacerbation of symptoms. The available data clearly demonstrate that inhibition of gastric emptying and stimulation of colonic transit is the most consistent pattern in the motility response of the GI tract to acute or short-term stress. Thus, one might propose that these alterations might play a pathophysiological role in dyspeptic symptoms and alterations in stool frequency and consistency in patients with stress-related functional GI disorders. Taken together, the above-mentioned studies suggest that the colonic motor response to stress is exaggerated in IBS. There is evidence that an increased emotional response is associated with this difference in colonic, and perhaps also gastric motor responses to certain stressors. However, almost no valid data are available so far from human studies addressing the question if differences in motility responses to stress between patients with functional GI disorders and healthy subjects are due to an altered stress response associated with an imbalance of the autonomic nervous system or increased stress susceptibility. We can summarize that in experimental animals the most consistent pattern of GI motor alterations induced by various psychological and physical stressors is that of delaying gastric emptying and accelerating colonic transit. Endogenous corticotropin-releasing factor (CRF) in the brain plays a significant role in the central nervous system mediation of stress-induced inhibition of upper GI and stimulation of lower GI motor function through activation of brain CRF receptors. The inhibition of gastric emptying by CRF may be mediated by interaction with the CRF-2 receptor, while CRF-1 receptors are involved in the colonic and anxiogenic responses to stress. Endogenous serotonin, peripherally released in response to stress, seems to be involved in stress- and central CRF-induced stimulation of colonic motility by acting on 5HT-3 receptors. Taken together, the limited data available from investigations in healthy subjects and patients with functional GI disorders provide some evidence that stress affects visceral sensitivity in humans. Acute psychological stress seems to facilitate increased sensitivity to experimental visceral stimuli, if the stressor induces a significant emotional change. In summary, studies in experimental animals suggest that stress-induced visceral hypersensitivity is centrally mediated by endogenous CRF and involvement of structures of the emotional motor system, e.g. the amygdala. Stress-induced activation or sensitization of mucosal mast cells in the GI tract seem to be involved in stress-associated alterations of visceral sensitivity.

show abstract

“…As an integral part of the nerveendocrine-immune network, mast cells participate in aspects of inflammation, and they also contribute to physiological regulation. Examples of the latter include the involvement of mast cells in cholecystokinin-induced disruption of the intestinal migrating motor complex (32) and in distension-induced and substance P-induced intestinal secretion (19). Some evidence attests to the importance of NT-mast cell interactions in inflammation.…”

Section: Discussionmentioning

confidence: 98%

Involvement of mast cells in basal and neurotensin-induced intestinal absorption of taurocholate in rats

Gui

Carraway

2004

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Neurotensin (NT), a hormone released from intestine by ingested fat, facilitates lipid digestion by stimulating pancreatic secretion and slowing the movement of chyme. In addition, NT can contract the gall bladder and enhance the enterohepatic circulation (EHC) of bile acids to promote micelle formation. Our recent finding that NT enhanced and an NT antagonist inhibited [(3)H]taurocholate ([(3)H]TC) absorption from proximal rat small intestine indicated a role for endogenous NT in the regulation of EHC. Here, we postulate the involvement of intestinal mast cells in the TC uptake process and in the stimulatory effect of NT. In anesthetized rats with the bile duct cannulated for bile collection, infusion of NT (10 pmol.kg(-1).min(-1)) enhanced the [(3)H]TC recovery rate from duodenojejunum by 2.2-fold. This response was abolished by pretreatment with mast cell stabilizers (cromoglycate, doxantrazole) and inhibitors of mast cell mediators (diphenhydramine, metergoline, zileuton). In contrast, mast cell degranulators (compound 48/80, substance P) and mast cell mediators (histamine, leukotriene C(4)) reproduced the effect of NT. N(G)-nitro-l-arginine methyl ester enhanced and l-arginine inhibited basal and NT-induced TC uptake, consistent with the known inhibitory effect of nitric oxide (NO) on mast cell reactivity. These results argue that basal and NT-stimulated TC uptake in rat jejunum are similarly dependent on mast cells, are largely mediated by release of mast cell mediators, and are subject to regulation by NO.

show abstract

Involvement of interleukin‐1, prostaglandins and mast cells in rectal distension‐induced colonic water secretion in rats

Cited by 12 publications

References 42 publications

Acute and chronic stress differently affect visceral sensitivity to rectal distension in female rats

Acute and chronic stress differently affect visceral sensitivity to rectal distension in female rats

Role of Stress in Functional Gastrointestinal Disorders

Involvement of mast cells in basal and neurotensin-induced intestinal absorption of taurocholate in rats

Contact Info

Product

Resources

About