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Sugamoto, Shinichi; Kawauch, Shoji; Furukawa, Osamu; Mimaki, Hiroshi; Takeuchi, Koji

doi:10.1023/a:1010603026913

Cited by 44 publications

(7 citation statements)

References 23 publications

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“…These data indicate that cells expressing elements essential for HCO − 3 secretion and the TRPM5-positive cells represent two distinct populations and that in the proximal corpus mucosa apparently brush cells are not the source for secreted bicarbonate. However, the observation that TRPM5-positive cells were frequently located in close proximity to CFTR-stained cells might be of functional relevance, especially in view of the previous findings that in other tissues secretion of bicarbonate is strongly affected by neighboring cells using prostaglandin as paracrine signal (Flemström et al, 1982; Takeuchi et al, 1999; Sugamoto et al, 2001; Akiba and Kaunitz, 2009). If such a scenario was also realized at the “gastric groove,” the brush cells need to comprise the enzyme prostaglandin-endoperoxide synthase, also called cyclooxygenase (COX) [reviewed by Kim (2011)].…”

Section: Resultsmentioning

confidence: 87%

Putative interaction of brush cells with bicarbonate secreting cells in the proximal corpus mucosa

Eberle¹,

Müller-Roth²,

Widmayer³

et al. 2013

Front. Physiol.

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The gastric epithelium is protected from the highly acidic luminal content by alkaline mucus which is secreted from specialized epithelial cells. In the stomach of mice strong secretion of alkaline fluid was observed at the “gastric groove,” the border between corpus and fundus mucosa. Since this region is characterized by numerous brush cells it was proposed that these cells might secrete alkaline solution as suggested for brush cells in the bile duct. In fact, it was found that in this region multiple cells express elements which are relevant for the secretion of bicarbonate, including carbonic anhydrase (CAII), the cystic fibrosis transmembrane conductance regulator (CFTR) and the Na+/H+ exchanger (NHE1). However, this cell population was distinct from brush cells which express the TRP-channel TRPM5 and are considered as putative sensory cells. The location of both cell populations in close proximity implies the possibility for a paracrine interaction. This view was substantiated by the finding that brush cells express prostaglandin synthase-1 (COX-1) and the neighboring cells a specific receptor type for prostaglandins. The notion that brush cells may be able to sense a local acidification was supported by the observation that they express the channel PKD1L3 which contributes to the acid responsiveness of gustatory sensory cells. The results support the concept that brush cells may sense the luminal content and influence via prostaglandins the secretion of alkaline solution.

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Section: Resultsmentioning

confidence: 87%

Putative interaction of brush cells with bicarbonate secreting cells in the proximal corpus mucosa

Eberle¹,

Müller-Roth²,

Widmayer³

et al. 2013

Front. Physiol.

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“…Both mediators are capable of modulating mucosal blood flow, mucus and bicarbonate secretions, and the repair of mucosal injury [14, 32, 33]. Konturek et al [34]reported that the healing of gastric ulcers induced by acetic acid was delayed and promoted by administration of NOS inhibitors and L -arginine, respectively.…”

Section: Discussionmentioning

confidence: 99%

Healing of Duodenal Ulcers Is Not Impaired by Indomethacin or Rofecoxib, the Selective COX-2 Inhibitor, in Rats

Araki¹,

Komoike²,

Matsumoto³

et al. 2002

Digestion

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Background/Aim: Studies have demonstrated an important role for endogenous PG and NO in the healing of chronic gastric ulcers. We investigated the effects of COX and NOS inhibitors on the healing of duodenal ulcers, in comparison with gastric ulcers, in rats. Methods: Gastric and duodenal ulcers were induced by serosal application of acetic acid (0.1 ml of 100% acetic acid) for 60 and 20 s, respectively. Indomethacin (a nonselective COX inhibitor) or rofecoxib (a selective COX-2 inhibitor) was given p.o. once daily for 14 days from 3 days after ulcer induction, while N^G-nitro-L-arginine methyl ester (L-NAME: a nonselective NOS inhibitor) or aminoguanidine (a relatively selective iNOS inhibitor) was given s.c. twice daily during this period. Results: Both gastric and duodenal ulcers induced by acetic acid healed spontaneously within 17 days to a minimal size. Daily administration of indomethacin or rofecoxib significantly delayed the healing of gastric but not duodenal ulcers. In contrast, the healing of both gastric and duodenal ulcers was delayed by repeated administration of either L-NAME or aminoguanidine. Ulceration markedly increased the PGE₂ content of the ulcerated mucosa in both the stomach and duodenum, and the increased PG biosynthetic response was inhibited by either indomethacin or rofecoxib in both tissues. The expression of both COX-2 and iNOS mRNAs was upregulated in the ulcerated mucosa of the stomach and duodenum. Conclusion: These results suggest that COX-2/PG is actively involved in the healing of gastric but not duodenal ulcers, although the mRNA for COX-2 is expressed in the duodenal mucosa after ulceration, as potently as in the gastric mucosa. In contrast, NO produced by both cNOS and iNOS plays a role in the healing of both gastric and duodenal ulcers.

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“…Although NO and PG affect acid-induced gastric mucosal hyperemia (45;46) and the gastric microcirculation (47), PG has no effect on the CRF 2 -mediated colonic hyperemia. Similarly, CRF 2 -mediated colonic hyperemia does not involve capsaicin-sensitive afferent fibers.…”

Section: Discussionmentioning

confidence: 99%

Peripheral Corticotropin-Releasing Factor Receptor Type 2 Activation Increases Colonic Blood Flow Through Nitric Oxide Pathway in Rats

2015

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Background Corticotropin-releasing factor (CRF) peptides exert profound effects on the secretomotor function of the gastrointestinal tract. Nevertheless, despite the presence of CRF peptides and receptors in colonic tissue, their influence on colonic blood flow (CBF) is unknown. Aim To determine the effect and mechanism of members of the CRF peptide family on CBF in isoflurane-anesthetized rats. Methods Proximal CBF was measured with laser Doppler flowmetry simultaneously with mean arterial blood pressure (MABP) measurement. Rats were injected with intravenous human/rat CRF (CRF1>CRF2 affinity), mouse urocortin 2 (mUcn2, selective CRF2 agonist) or sauvagine (SVG, CRF2>CRF1 affinity) at 1 – 30 μg/kg. The nitric oxide (NO) synthase inhibitor, L-NAME (3 mg/kg, iv), the cyclooxygenase inhibitor, indomethacin (Indo, 5 mg/kg, ip) or selective CRF2 antagonist, astressin2-B (Ast2B, 50 μg/kg, iv) was given before SVG injection (10 μg/kg, iv). Results SVG and mUcn2 dose-dependently increased CBF while decreasing MABP and colonic vascular resistance (CVR). CRF had no effect on CBF, but increased CVR. The hyperemic effect of SVG was inhibited by L-NAME but not by Indo, whereas hypotension was partially reduced by L-NAME. Sensory denervation had no effect on SVG-induced changes. Ast2B inhibited SVG-induced hyperemia and decreased CVR, and partially reduced the hypotension. Conclusions Peripheral CRF2 activation induces colonic hyperemia through NO synthesis, without involving prostaglandin synthesis or sensory nerve activation, suggesting a direct action on the endothelium and myenteric neurons. Members of the CRF peptide family may protect the colonic mucosal via the activation of the CRF2 receptor.

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Cited by 44 publications

References 23 publications

Putative interaction of brush cells with bicarbonate secreting cells in the proximal corpus mucosa

Putative interaction of brush cells with bicarbonate secreting cells in the proximal corpus mucosa

Healing of Duodenal Ulcers Is Not Impaired by Indomethacin or Rofecoxib, the Selective COX-2 Inhibitor, in Rats

Peripheral Corticotropin-Releasing Factor Receptor Type 2 Activation Increases Colonic Blood Flow Through Nitric Oxide Pathway in Rats

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