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Article: Combined effects of endothelin-1 and platelet activating factor on rat aorta vasoconstriction

TitleCombined effects of endothelin-1 and platelet activating factor on rat aorta vasoconstriction
Authors
Issue Date1998
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
Faseb Journal, 1998, v. 12 n. 5, p. A1001 How to Cite?
AbstractEndothelin (ET-1) is a potent vasoconstrictor derived from endothelial cells. Platelet activating actor (PAF) is a phospholipid mediator synthesized by a variety of cell types. ET-1 and PAF may play important roles in modulating vasomotor tone and blood pressure. Little is known about their combined vasoconstrictive effects. The objective of this study was to investigate the combined effects of ET-1 and PAF on the rat aorta. Thoracic aortic rings of rats were suspended in organ baths and ET-1 (5nM) and PAF (10nM) were added. Contractions of aortic rings were measured by transducers. PAF significantly potentiated and prolonged ET-1 induced vasoconstriction which was endothelium-independent. However, PAF alone did not induce constriction of aortic ring. Indomethacin (cyclooxygenase inhibitor) did not inhibit ET-1 induced vasoconstriction but significantly inhibited PAF potentiated ET-1 induced vasoconstriction. When phosphoramidon (an inhibitor of endothelin converting enzyme) was added to the organ bath, the combined effect of PAF and ET-1 on vasoconstriction was not affected. This result suggests that PAF potentiated vasoconstriction is not due to the synthesis of ET-1. In conclusion, our results demonstrate that PAF potentiated ET-1 induced vasoconstriction may take part in aortic smooth muscle cells via the cyclooxygenase pathway.
Persistent Identifierhttp://hdl.handle.net/10722/171349
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775

 

DC FieldValueLanguage
dc.contributor.authorKoon, MHWen_US
dc.contributor.authorMan, RYKen_US
dc.contributor.authorKarmin, Oen_US
dc.date.accessioned2012-10-30T06:13:31Z-
dc.date.available2012-10-30T06:13:31Z-
dc.date.issued1998en_US
dc.identifier.citationFaseb Journal, 1998, v. 12 n. 5, p. A1001en_US
dc.identifier.issn0892-6638en_US
dc.identifier.urihttp://hdl.handle.net/10722/171349-
dc.description.abstractEndothelin (ET-1) is a potent vasoconstrictor derived from endothelial cells. Platelet activating actor (PAF) is a phospholipid mediator synthesized by a variety of cell types. ET-1 and PAF may play important roles in modulating vasomotor tone and blood pressure. Little is known about their combined vasoconstrictive effects. The objective of this study was to investigate the combined effects of ET-1 and PAF on the rat aorta. Thoracic aortic rings of rats were suspended in organ baths and ET-1 (5nM) and PAF (10nM) were added. Contractions of aortic rings were measured by transducers. PAF significantly potentiated and prolonged ET-1 induced vasoconstriction which was endothelium-independent. However, PAF alone did not induce constriction of aortic ring. Indomethacin (cyclooxygenase inhibitor) did not inhibit ET-1 induced vasoconstriction but significantly inhibited PAF potentiated ET-1 induced vasoconstriction. When phosphoramidon (an inhibitor of endothelin converting enzyme) was added to the organ bath, the combined effect of PAF and ET-1 on vasoconstriction was not affected. This result suggests that PAF potentiated vasoconstriction is not due to the synthesis of ET-1. In conclusion, our results demonstrate that PAF potentiated ET-1 induced vasoconstriction may take part in aortic smooth muscle cells via the cyclooxygenase pathway.en_US
dc.languageengen_US
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_US
dc.relation.ispartofFASEB Journalen_US
dc.titleCombined effects of endothelin-1 and platelet activating factor on rat aorta vasoconstrictionen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-33749366455en_US
dc.identifier.volume12en_US
dc.identifier.issue5en_US
dc.identifier.spageA1001en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKoon, MHW=14825235800en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridKarmin, O=6604083266en_US

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