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Article: Raloxifene prevents endothelial dysfunction in aging ovariectomized female rats

TitleRaloxifene prevents endothelial dysfunction in aging ovariectomized female rats
Authors
KeywordsArteries
Endothelial function
Hormones
Vasoconstriction/dilation
Issue Date2006
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vph
Citation
Vascular Pharmacology, 2006, v. 44 n. 5, p. 290-298 How to Cite?
AbstractLack of an appropriate animal model has delayed the better understanding of mechanisms related to higher cardiovascular risk in women after menopause. The aging female rat may share some menopausal changes observed in women. However, most studies have attempted to mimic menopause by ovariectomizing young (6-12 weeks old) animals without taking into accounts the influence of aging and of declining ovarian function. Therefore, the present study examined changes in vascular reactivity in the aging (15 months old) female rat after ovariectomy and the effects of chronic raloxifene therapy on vascular reactivity and eNOS protein expression. Aortic rings were prepared from the three experimental groups of rats: sham-operated control, ovariectomized and ovariectomized aging rats receiving daily oral administration of raloxifene for 3 months. Aortic rings were suspended in organ baths for the measurement of isometric tension. Rings with endothelium contracted significantly more to phenylephrine after inhibition of nitric oxide/cyclic GMP-signaling pathway by l-NAME or ODQ (as an index of basal nitric oxide release) in control and raloxifene-treated ovariectomized rats than in ovariectomized rats. This effect was abolished upon mechanical removal of the endothelium. Phenylephrine induced greater contractions only in rings with endothelium from ovariectomized rats as compared with control rats and raloxifene treatment normalized this response. In the presence of l-NAME or ODQ, phenylephrine-induced contraction was similar in rings from the three groups. Rings relaxed more to thapsigargin and acetylcholine in raloxifene-treated ovariectomized rats than in ovariectomized rats. There was no significant difference in aortic eNOS protein contents among the different groups. These results suggest that chronic oral administration of raloxifene to aging ovariectomized female rats augmented the bioavailability of endothelial nitric oxide in isolated aortic rings without altering eNOS protein levels. © 2006 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80267
ISSN
2015 Impact Factor: 2.5
2015 SCImago Journal Rankings: 1.204
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, CMen_HK
dc.contributor.authorYao, Xen_HK
dc.contributor.authorAu, CLen_HK
dc.contributor.authorTsang, SYen_HK
dc.contributor.authorFung, KPen_HK
dc.contributor.authorLaher, Ien_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorHuang, Yen_HK
dc.date.accessioned2010-09-06T08:04:24Z-
dc.date.available2010-09-06T08:04:24Z-
dc.date.issued2006en_HK
dc.identifier.citationVascular Pharmacology, 2006, v. 44 n. 5, p. 290-298en_HK
dc.identifier.issn1537-1891en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80267-
dc.description.abstractLack of an appropriate animal model has delayed the better understanding of mechanisms related to higher cardiovascular risk in women after menopause. The aging female rat may share some menopausal changes observed in women. However, most studies have attempted to mimic menopause by ovariectomizing young (6-12 weeks old) animals without taking into accounts the influence of aging and of declining ovarian function. Therefore, the present study examined changes in vascular reactivity in the aging (15 months old) female rat after ovariectomy and the effects of chronic raloxifene therapy on vascular reactivity and eNOS protein expression. Aortic rings were prepared from the three experimental groups of rats: sham-operated control, ovariectomized and ovariectomized aging rats receiving daily oral administration of raloxifene for 3 months. Aortic rings were suspended in organ baths for the measurement of isometric tension. Rings with endothelium contracted significantly more to phenylephrine after inhibition of nitric oxide/cyclic GMP-signaling pathway by l-NAME or ODQ (as an index of basal nitric oxide release) in control and raloxifene-treated ovariectomized rats than in ovariectomized rats. This effect was abolished upon mechanical removal of the endothelium. Phenylephrine induced greater contractions only in rings with endothelium from ovariectomized rats as compared with control rats and raloxifene treatment normalized this response. In the presence of l-NAME or ODQ, phenylephrine-induced contraction was similar in rings from the three groups. Rings relaxed more to thapsigargin and acetylcholine in raloxifene-treated ovariectomized rats than in ovariectomized rats. There was no significant difference in aortic eNOS protein contents among the different groups. These results suggest that chronic oral administration of raloxifene to aging ovariectomized female rats augmented the bioavailability of endothelial nitric oxide in isolated aortic rings without altering eNOS protein levels. © 2006 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/vphen_HK
dc.relation.ispartofVascular Pharmacologyen_HK
dc.subjectArteriesen_HK
dc.subjectEndothelial functionen_HK
dc.subjectHormonesen_HK
dc.subjectVasoconstriction/dilationen_HK
dc.titleRaloxifene prevents endothelial dysfunction in aging ovariectomized female ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.vph.2005.12.005en_HK
dc.identifier.pmid16542882-
dc.identifier.scopuseid_2-s2.0-33646124946en_HK
dc.identifier.hkuros119607en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646124946&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue5en_HK
dc.identifier.spage290en_HK
dc.identifier.epage298en_HK
dc.identifier.isiWOS:000237719100005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, CM=36631360800en_HK
dc.identifier.scopusauthoridYao, X=7402529434en_HK
dc.identifier.scopusauthoridAu, CL=7102805672en_HK
dc.identifier.scopusauthoridTsang, SY=7102255908en_HK
dc.identifier.scopusauthoridFung, KP=7202934739en_HK
dc.identifier.scopusauthoridLaher, I=7005431686en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK

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