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pubmed-article:18212515pubmed:abstractTextThe majority of prostaglandins (PGs) are known to induce intestinal fluid secretion (enteropooling). In contrast, PGD(2) has been demonstrated to inhibit fluid secretion induced by other PGs. This study was aimed to investigate, by the use of selective agonists/antagonists, which type of PGD(2) receptor mediates this inhibitory effect. The DP1 agonist BW245C dose-dependently inhibited the enteropooling effect of 16,16-dimethyl-PGE(2). This inhibition was counteracted by the DP1 antagonist BWA868C. In contrast, the CRTH2 receptor does not seem to be involved in the anti-enteropooling effect of PGD(2), since the selective agonists 13,14-dihydro-15-keto-PGD(2) and 15(R)-15-methyl-PGD(2) were without effect. Therefore, our results suggest that the inhibitory effect of PGD(2) in the small intestine is mediated via activation of the DP1 receptor.lld:pubmed
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pubmed-article:18212515pubmed:authorpubmed-author:PeskarB ABAlld:pubmed
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pubmed-article:18212515pubmed:copyrightInfoCopyright 2008 S. Karger AG, Basel.lld:pubmed
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pubmed-article:18212515pubmed:volume81lld:pubmed
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pubmed-article:18212515pubmed:pagination236-40lld:pubmed
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pubmed-article:18212515pubmed:articleTitleCRTH2 is not involved in the anti-enteropooling effect of PGD2 in the small intestine.lld:pubmed
pubmed-article:18212515pubmed:affiliationInstitute of Experimental and Clinical Pharmacology, Medical University Graz, Graz, Austria.lld:pubmed
pubmed-article:18212515pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18212515pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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