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Article: Raloxifene modulates pulmonary vascular reactivity in spontaneously hypertensive rats

TitleRaloxifene modulates pulmonary vascular reactivity in spontaneously hypertensive rats
Authors
KeywordsEndothelium
Pulmonary arteries
Raloxifene
Spontaneously hypertensive rat
Vasoconstriction
Issue Date2007
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 2007, v. 49 n. 6, p. 355-361 How to Cite?
AbstractSelective estrogen receptor modulators (SERMs) reduce vascular tone in the systemic circulation. Their effects on the pulmonary circulation are unknown. The present study examined the effect of oral treatment with raloxifene (a second-generation SERM) on vasomotor reactivity in pulmonary arteries from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Pulmonary arterial rings were suspended in a multi-channel myograph, and changes in isometric tension were measured. WKY rings constricted less to U46619 than SHR rings, and the difference was eliminated after chronic treatment with raloxifene. More contraction to U46619 was obtained after inhibition of nitric oxide synthase (NOS) by L-NAME (as an index of basal NO release) in raloxifene-treated than in control SHR rings. Less U46619-induced contraction after raloxifene treatment occurred only in SHR rings with endothelium, and this effect was abolished upon removal of the endothelium. Raloxifene treatment did not enhance the contribution of basal NO to U46619-induced constriction in WKY rings. Raloxifene treatment did not modify endothelium-dependent relaxation to acetylcholine and endothelium-independent relaxation to nifedipine. The reduced relaxing sensitivity to sodium nitroprusside (SNP) in SHR rings was normalized by raloxifene treatment. Raloxifene treatment reduced CaCl2-induced tone in SHR but not in WKY rings. The results show that chronic treatment with raloxifene could improve pulmonary vascular function in hypertensive animals by (1) increasing basal NO release, (2) reducing vascular smooth muscle tone, and (3) improving the effect of NO on vascular smooth muscle in SHR. In contrast, raloxifene has little effect on vascular reactivity in pulmonary arteries from normotensive WKY rats. © 2007 Lippincott Williams & Wilkins, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/134681
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, YCen_HK
dc.contributor.authorLeung, FPen_HK
dc.contributor.authorYao, Xen_HK
dc.contributor.authorLau, CWen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorHuang, Yen_HK
dc.date.accessioned2011-07-05T08:24:16Z-
dc.date.available2011-07-05T08:24:16Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 2007, v. 49 n. 6, p. 355-361en_HK
dc.identifier.issn0160-2446en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134681-
dc.description.abstractSelective estrogen receptor modulators (SERMs) reduce vascular tone in the systemic circulation. Their effects on the pulmonary circulation are unknown. The present study examined the effect of oral treatment with raloxifene (a second-generation SERM) on vasomotor reactivity in pulmonary arteries from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Pulmonary arterial rings were suspended in a multi-channel myograph, and changes in isometric tension were measured. WKY rings constricted less to U46619 than SHR rings, and the difference was eliminated after chronic treatment with raloxifene. More contraction to U46619 was obtained after inhibition of nitric oxide synthase (NOS) by L-NAME (as an index of basal NO release) in raloxifene-treated than in control SHR rings. Less U46619-induced contraction after raloxifene treatment occurred only in SHR rings with endothelium, and this effect was abolished upon removal of the endothelium. Raloxifene treatment did not enhance the contribution of basal NO to U46619-induced constriction in WKY rings. Raloxifene treatment did not modify endothelium-dependent relaxation to acetylcholine and endothelium-independent relaxation to nifedipine. The reduced relaxing sensitivity to sodium nitroprusside (SNP) in SHR rings was normalized by raloxifene treatment. Raloxifene treatment reduced CaCl2-induced tone in SHR but not in WKY rings. The results show that chronic treatment with raloxifene could improve pulmonary vascular function in hypertensive animals by (1) increasing basal NO release, (2) reducing vascular smooth muscle tone, and (3) improving the effect of NO on vascular smooth muscle in SHR. In contrast, raloxifene has little effect on vascular reactivity in pulmonary arteries from normotensive WKY rats. © 2007 Lippincott Williams & Wilkins, Inc.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_HK
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_HK
dc.subjectEndotheliumen_HK
dc.subjectPulmonary arteriesen_HK
dc.subjectRaloxifeneen_HK
dc.subjectSpontaneously hypertensive raten_HK
dc.subjectVasoconstrictionen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBlood Pressure - drug effectsen_HK
dc.subject.meshEndothelium, Vascular - drug effectsen_HK
dc.subject.meshHypertension - physiopathologyen_HK
dc.subject.meshLung - blood supplyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshPulmonary Artery - drug effectsen_HK
dc.subject.meshRaloxifene - pharmacologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Inbred SHRen_HK
dc.subject.meshRats, Inbred WKYen_HK
dc.subject.meshSelective Estrogen Receptor Modulators - pharmacologyen_HK
dc.subject.meshVasoconstriction - drug effectsen_HK
dc.titleRaloxifene modulates pulmonary vascular reactivity in spontaneously hypertensive ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, YC: yauchi@graduate.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityChan, YC=rp01502en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/FJC.0b013e318046f329en_HK
dc.identifier.pmid17577099-
dc.identifier.scopuseid_2-s2.0-34347258416en_HK
dc.identifier.hkuros136334-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34347258416&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume49en_HK
dc.identifier.issue6en_HK
dc.identifier.spage355en_HK
dc.identifier.epage361en_HK
dc.identifier.isiWOS:000247688500003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, YC=7403676116en_HK
dc.identifier.scopusauthoridLeung, FP=8615375300en_HK
dc.identifier.scopusauthoridYao, X=7402529434en_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridHuang, Y=7501573013en_HK

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