Document Detail

Involvement of prostaglandin E receptor EP3 subtype and prostacyclin IP receptor in decreased acid response in damaged stomach.
MedLine Citation:
PMID:  17928639     Owner:  NLM     Status:  MEDLINE    
We investigated the roles of cyclooxygenase (COX) isozymes and prostaglandin E (PGE) receptor EP1 and EP3 subtypes or prostacyclin IP receptors in the decrease in acid secretion in the damaged mouse stomach. Male C57/BL6 mice, both wild type and animals lacking EP1, EP3, or IP receptors, were used after 18 h of fasting. Under urethane anesthesia, the stomach was mounted on an ex-vivo chamber and perfused with saline, and acid secretion as well as transmucosal potential difference (PD) was measured before and after exposure to 20 mM taurocholate Na (TC) for 20 min. Indomethacin, SC-560 or rofecoxib was given i.d. 30 min before TC. Mucosal exposure to TC in wild-type mice caused a reduction in PD, followed by decrease in acid secretion. Indomethacin attenuated the decrease in acid secretion after exposure to TC in wild-type mice, an effect mimicked by SC-560 but not rofecoxib, yet none of these drugs affected the decrease in PD. An altered acid response after exposure to TC was similarly observed in EP1 (-/-) mice but mitigated in mice lacking either EP3 or IP receptors, although a decrease in PD was observed in all groups. Furthermore, the decreased acid response was also attenuated by prior administration of the EP3- but not EP1- antagonist. Mucosal levels of PGE(2) and 6-keto PGF(1a) increased after exposure to TC in all groups of mice. In conclusion, the decrease in acid secretion in the damaged stomach is mediated by endogenous PGs derived from COX-1, through PGE(2)/EP3 receptors and prostacyclin/IP receptors.
H Nishio; S Terashima; M Nakashima; E Aihara; K Takeuchi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of physiology and pharmacology : an official journal of the Polish Physiological Society     Volume:  58     ISSN:  0867-5910     ISO Abbreviation:  J. Physiol. Pharmacol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-10-11     Completed Date:  2007-12-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9114501     Medline TA:  J Physiol Pharmacol     Country:  Poland    
Other Details:
Languages:  eng     Pagination:  407-21     Citation Subset:  IM    
Department of Pharmacology and Experimental Therapeutic, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto, Japan.
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MeSH Terms
6-Ketoprostaglandin F1 alpha / analysis,  metabolism
Bicyclo Compounds / pharmacology
Cyclooxygenase 1 / metabolism
Cyclooxygenase 2 / drug effects,  metabolism
Cyclooxygenase 2 Inhibitors / pharmacology
Dinoprostone / analysis,  metabolism
Gastric Acid / secretion*
Gastric Acidity Determination
Gastric Mucosa / drug effects,  metabolism,  physiology
Hexanoic Acids / pharmacology
Hydrogen-Ion Concentration
Indomethacin / pharmacology
Lactones / pharmacology
Membrane Potentials / drug effects
Membrane Proteins / antagonists & inhibitors,  metabolism
Mice, Inbred C57BL
Mice, Knockout
Pyrazoles / pharmacology
Receptors, Prostaglandin / antagonists & inhibitors,  genetics,  metabolism*
Receptors, Prostaglandin E / antagonists & inhibitors,  genetics,  metabolism*
Stomach Diseases / metabolism*,  physiopathology
Sulfones / pharmacology
Taurocholic Acid / pharmacology
Reg. No./Substance:
0/Bicyclo Compounds; 0/Cyclooxygenase 2 Inhibitors; 0/Hexanoic Acids; 0/Lactones; 0/Membrane Proteins; 0/ONO 8711; 0/Ptgir protein, mouse; 0/Pyrazoles; 0/Receptors, Prostaglandin; 0/Receptors, Prostaglandin E; 0/SC 560; 0/Sulfones; 0/prostaglandin EP3 receptor; 0/rofecoxib; 363-24-6/Dinoprostone; 53-86-1/Indomethacin; 58962-34-8/6-Ketoprostaglandin F1 alpha; 81-24-3/Taurocholic Acid; EC 1.14.99.-/Ptgs2 protein, mouse; EC 1; EC 2; EC protein, mouse

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