| Gastric ulcerogenic responses following barrier disruption in knockout mice lacking prostaglandin EP1 receptors. | |
| | |
MedLine Citation:
|
PMID: 11966527 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND/AIMS: Endogenous prostaglandins (PGs) are considered to play a pivotal role in maintaining the mucosal integrity of the stomach after injury. In the present study, we evaluated the mucosal ulcerogenic and mucosal blood flow (GMBF) responses in the stomach after damage by taurocholate (TC) in knockout mice lacking EP1 or EP3 receptors. METHODS: Under urethane anaesthesia, a mouse stomach was mounted in an ex vivo chamber, exposed to 20 mmol/L TC for 20 min and treated with 20 mmol/L HCl before and after TC. GMBF was measured with a laser Doppler flowmeter. RESULTS: Mucosal exposure to TC in wild-type mice caused a marked decrease in potential difference (PD), followed by an increase in H+ loss and GMBF. The decreased PD was gradually normalized after removal of TC from the chamber, with minimal damage in the mucosa 1 h after TC treatment. This hyperaemic response was inhibited by indomethacin, resulting in severe lesions in the mucosa without any change in PD or H+ loss. None of these responses induced by TC were altered in EP3-/- mice. However, in mice lacking EP1 receptors, TC treatment did not increase GMBF, despite causing PD reduction and acid loss, and resulted in severe damage in the mucosa. These responses were closely similar to those observed in animals pretreated with ONO-8711, a EP1 receptor antagonist. Mucosal PGE2 content was significantly increased after TC, similarly in all groups of mice. CONCLUSION: These results confirm a mediator role for PGE2 in gastric hyperaemic response following mucosal exposure to TC and suggest that endogenous PGs may contribute to maintaining mucosal integrity after barrier disruption, mainly through activation of the EP1 receptor subtype. |
| | |
Authors:
|
K Takeuchi; Y Ogawa; S Kagawa; H Ukawa |
Related Documents
:
|
10334817 - Type 2 bradykinin-receptor antagonism does not modify kinin or angiotensin peptide levels. 21971867 - Neuropeptide y y1 receptor hippocampal overexpression via viral vectors is associated w... 8518937 - The effects of capsaicin, bradykinin, pge2 and cicaprost on the discharge of articular ... 22269807 - Hippocampal ampa-type receptor complexes containing glur3 and glur4 are paralleling tra... 11707587 - Evidence that androgens are the primary steroids produced by xenopus laevis ovaries and... 3575347 - Chronic autoreceptor blockade and neuroleptic-induced dopamine receptor hypersensitivity. |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Alimentary pharmacology & therapeutics Volume: 16 Suppl 2 ISSN: 0269-2813 ISO Abbreviation: Aliment. Pharmacol. Ther. Publication Date: 2002 Apr |
Date Detail:
|
Created Date: 2002-04-22 Completed Date: 2002-07-15 Revised Date: 2006-11-15 |
Medline Journal Info:
|
Nlm Unique ID: 8707234 Medline TA: Aliment Pharmacol Ther Country: England |
Other Details:
|
Languages: eng Pagination: 74-82 Citation Subset: IM |
Affiliation:
|
Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Japan. takeuchi@mb.kyoto-phu.ac.jp |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Bicyclo Compounds / pharmacology Cytoprotection Dinoprostone / biosynthesis* Disease Models, Animal Gastric Mucosa / blood supply, drug effects, metabolism* Hexanoic Acids / pharmacology Indomethacin / pharmacology Mice Mice, Knockout Receptors, Prostaglandin E / antagonists & inhibitors, genetics, metabolism* Regional Blood Flow / drug effects Stomach Ulcer / chemically induced, metabolism* Taurocholic Acid / toxicity |
| Chemical | |
Reg. No./Substance:
|
0/Bicyclo Compounds; 0/Hexanoic Acids; 0/ONO 8711; 0/Receptors, Prostaglandin E; 0/prostanoid receptor EP1; 363-24-6/Dinoprostone; 53-86-1/Indomethacin; 81-24-3/Taurocholic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Effect of PPARgamma ligands on the viability of gastric epithelial cells.
Next Document: Inhibition of proliferation of gastric epithelial cells by a cyclooxygenase 2 inhibitor, JTE522, is ...