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Conference Paper: RHO kinase and endothelium-dependent contractions in the SHR and WKY aorta

TitleRHO kinase and endothelium-dependent contractions in the SHR and WKY aorta
Authors
Issue Date2008
PublisherWiley-Blackwell Publishing Ltd.
Citation
The 5th International EDHF Symposium, Tampere, Finland, 24-27 June 2008. In Basic & Clinical Pharmacology & Toxicology, 2008, v. 102 suppl. 1, p. 55 How to Cite?
AbstractThe release of endothelium-dependent contracting factor (EDCF) isaugmented in the aorta of the spontaneously hypertensive (SHR)compared to that of the Wistar Kyoto (WKY) rats. EDCF eventuallyactivates TP receptors of the vascular smooth muscle cells. The presentstudy was designed to investigate the role of Rho kinase in EDCF-mediated responses. Quiescent aortic rings with endothelium of SHRand WKY were contracted with acetylcholine or the calcium ionophoreA23187 in the presence of L-NAME, isometric tension was measured.Two chemically distinct Rho kinase inhibitors, Y27632 and HA1077,reduced the contractions to both agonists, suggesting the importance ofRho kinase in EDCF-mediated responses. To study the role of Rhokinase in vascular smooth muscle cells, contractions to the TP receptoragonist U46619 or prostaglandin F2awere obtained in rings withoutendothelium of SHR and WKY aorta. The concentration response curveswere comparable in the two strains. The Rho kinase inhibitors Y27632and HA1077 inhibited the contractions to both U46619 and prostaglan-din F2a, but to a lesser extent than the endothelium-dependentcontractions to acetylcholine and A23187. These results suggest thatRho kinase is involved both in the release and the action of EDCF.
DescriptionPoster Presentations
Persistent Identifierhttp://hdl.handle.net/10722/106820
ISSN

 

DC FieldValueLanguage
dc.contributor.authorChan, KYCen_HK
dc.contributor.authorMak, JCWen_HK
dc.contributor.authorMan, RYKen_HK
dc.contributor.authorVanhoutte, PMGRen_HK
dc.date.accessioned2010-09-25T23:31:46Z-
dc.date.available2010-09-25T23:31:46Z-
dc.date.issued2008en_HK
dc.identifier.citationThe 5th International EDHF Symposium, Tampere, Finland, 24-27 June 2008. In Basic & Clinical Pharmacology & Toxicology, 2008, v. 102 suppl. 1, p. 55en_HK
dc.identifier.issn1742-7843-
dc.identifier.urihttp://hdl.handle.net/10722/106820-
dc.descriptionPoster Presentations-
dc.description.abstractThe release of endothelium-dependent contracting factor (EDCF) isaugmented in the aorta of the spontaneously hypertensive (SHR)compared to that of the Wistar Kyoto (WKY) rats. EDCF eventuallyactivates TP receptors of the vascular smooth muscle cells. The presentstudy was designed to investigate the role of Rho kinase in EDCF-mediated responses. Quiescent aortic rings with endothelium of SHRand WKY were contracted with acetylcholine or the calcium ionophoreA23187 in the presence of L-NAME, isometric tension was measured.Two chemically distinct Rho kinase inhibitors, Y27632 and HA1077,reduced the contractions to both agonists, suggesting the importance ofRho kinase in EDCF-mediated responses. To study the role of Rhokinase in vascular smooth muscle cells, contractions to the TP receptoragonist U46619 or prostaglandin F2awere obtained in rings withoutendothelium of SHR and WKY aorta. The concentration response curveswere comparable in the two strains. The Rho kinase inhibitors Y27632and HA1077 inhibited the contractions to both U46619 and prostaglan-din F2a, but to a lesser extent than the endothelium-dependentcontractions to acetylcholine and A23187. These results suggest thatRho kinase is involved both in the release and the action of EDCF.-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.-
dc.relation.ispartofBasic & Clinical Pharmacology & Toxicologyen_HK
dc.titleRHO kinase and endothelium-dependent contractions in the SHR and WKY aortaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailMak, JCW: judymak@HKUCC.hku.hken_HK
dc.identifier.emailMan, RYK: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_HK
dc.identifier.authorityMak, JCW=rp00352en_HK
dc.identifier.authorityMan, RYK=rp00236en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1742-7843.2008.00263.x-
dc.identifier.hkuros152536en_HK
dc.identifier.volume102en_HK
dc.identifier.issuesuppl. 1en_HK
dc.identifier.spage55en_HK
dc.identifier.epage55-

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