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Article: The role of prostaglandin E and thromboxane-prostanoid receptors in the response to prostaglandin E2 in the aorta of Wistar Kyoto rats and spontaneously hypertensive rats

TitleThe role of prostaglandin E and thromboxane-prostanoid receptors in the response to prostaglandin E2 in the aorta of Wistar Kyoto rats and spontaneously hypertensive rats
Authors
KeywordsEndothelial factors
Endothelial function
Endothelium-derived contracting factor
Vasoconstriction/dilation
Issue Date2008
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2008, v. 78 n. 1, p. 130-138 How to Cite?
AbstractAims: The present study examined the hypothesis that prostaglandin E 2 (PGE2) through activation of prostaglandin E (EP) receptor contributes to endothelium-dependent contractions. Methods and results: Western blotting revealed that the protein expression of EP1 receptor was significantly down-regulated in the aorta of the spontaneously hypertensive rat (SHR), but there was no significant difference in the expression of EP2, EP4, and total EP3 receptors between preparations of Wistar Kyoto rats (WKY) and SHR. Isometric tension studies showed that low concentrations of PGE2 caused endothelium-dependent relaxations in WKY but not in aortas of the SHR. High concentrations of PGE2 evoked contractions predominately through the activation of thromboxane-prostanoid (TP) receptors in the WKY, but involves the dual activation EP and TP receptors in the SHR. SQ29,548, BAYu3405 and Terutroban (TP receptor antagonists), and AH6809 (non-selective EP receptor antagonist) abolished, while SC19220 (preferential EP1 receptor antagonist) did not inhibit endothelium-dependent contractions. Both SC19220 and AH6809 significantly inhibited contractions to U46619 (TP receptor agonist). Conclusion: The present study demonstrates that the contraction caused by PGE2 in the SHR aorta is dependent on the activation of EP1 and TP receptors, but that endothelium-dependent contractions do not require the former. Thus, PGE2 is unlikely to be an endothelium-derived contracting factor in this artery. The ability of AH6809 to inhibit endothelium-dependent contractions can be attributed to its partial antagonism at TP receptors. Nevertheless, the impairment of PGE2-mediated relaxation may contribute to endothelial dysfunction in the aorta of the SHR. © The Author 2007.
Persistent Identifierhttp://hdl.handle.net/10722/91743
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorJensen, BLen_HK
dc.contributor.authorSkott, Oen_HK
dc.contributor.authorLeung, GPHen_HK
dc.contributor.authorFeletou, Men_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-17T10:25:14Z-
dc.date.available2010-09-17T10:25:14Z-
dc.date.issued2008en_HK
dc.identifier.citationCardiovascular Research, 2008, v. 78 n. 1, p. 130-138en_HK
dc.identifier.issn0008-6363en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91743-
dc.description.abstractAims: The present study examined the hypothesis that prostaglandin E 2 (PGE2) through activation of prostaglandin E (EP) receptor contributes to endothelium-dependent contractions. Methods and results: Western blotting revealed that the protein expression of EP1 receptor was significantly down-regulated in the aorta of the spontaneously hypertensive rat (SHR), but there was no significant difference in the expression of EP2, EP4, and total EP3 receptors between preparations of Wistar Kyoto rats (WKY) and SHR. Isometric tension studies showed that low concentrations of PGE2 caused endothelium-dependent relaxations in WKY but not in aortas of the SHR. High concentrations of PGE2 evoked contractions predominately through the activation of thromboxane-prostanoid (TP) receptors in the WKY, but involves the dual activation EP and TP receptors in the SHR. SQ29,548, BAYu3405 and Terutroban (TP receptor antagonists), and AH6809 (non-selective EP receptor antagonist) abolished, while SC19220 (preferential EP1 receptor antagonist) did not inhibit endothelium-dependent contractions. Both SC19220 and AH6809 significantly inhibited contractions to U46619 (TP receptor agonist). Conclusion: The present study demonstrates that the contraction caused by PGE2 in the SHR aorta is dependent on the activation of EP1 and TP receptors, but that endothelium-dependent contractions do not require the former. Thus, PGE2 is unlikely to be an endothelium-derived contracting factor in this artery. The ability of AH6809 to inhibit endothelium-dependent contractions can be attributed to its partial antagonism at TP receptors. Nevertheless, the impairment of PGE2-mediated relaxation may contribute to endothelial dysfunction in the aorta of the SHR. © The Author 2007.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_HK
dc.relation.ispartofCardiovascular Researchen_HK
dc.subjectEndothelial factorsen_HK
dc.subjectEndothelial functionen_HK
dc.subjectEndothelium-derived contracting factoren_HK
dc.subjectVasoconstriction/dilationen_HK
dc.titleThe role of prostaglandin E and thromboxane-prostanoid receptors in the response to prostaglandin E2 in the aorta of Wistar Kyoto rats and spontaneously hypertensive ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authorityLeung, GPH=rp00234en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/cvr/cvm112en_HK
dc.identifier.pmid18093985-
dc.identifier.scopuseid_2-s2.0-41149175178en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-41149175178&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume78en_HK
dc.identifier.issue1en_HK
dc.identifier.spage130en_HK
dc.identifier.epage138en_HK
dc.identifier.eissn1755-3245-
dc.identifier.isiWOS:000254793300018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridJensen, BL=35502338900en_HK
dc.identifier.scopusauthoridSkott, O=7005724990en_HK
dc.identifier.scopusauthoridLeung, GPH=35963668200en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK
dc.identifier.scopusauthoridMan, RYK=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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