File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Raloxifene improves vascular reactivity in pressurized septal coronary arteries of ovariectomized hamsters fed cholesterol diet

TitleRaloxifene improves vascular reactivity in pressurized septal coronary arteries of ovariectomized hamsters fed cholesterol diet
Authors
KeywordsCholesterol
Hamster
Myogenic constriction
Ovariectomy
Raloxifene
Septal coronary arteries
Issue Date2012
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618
Citation
Pharmacological Research, 2012, v. 65 n. 2, p. 182-188 How to Cite?
AbstractAlthough vascular effects of selective estrogen receptor modulators (SERMs) have been extensively examined in conduit arteries, whether SERMs could favorably modulate myogenic response in resistance arteries is unknown. The impact of raloxifene therapy and cholesterol diet on myogenic constriction during estrogen deficiency is unresolved. This study investigated changes in vascular reactivity and myogenic responses in female ovariectomized (Ovx) hamsters fed high-cholesterol diet (HCD) with and without chronic treatment of raloxifene. Functional studies were performed on hamster septal coronary arteries cannulated in a pressure myograph. Acetylcholine (ACh)-induced dilatation was reduced in arteries from cholesterol-fed Ovx hamsters, but not in those from cholesterol-fed hamsters, while pressure-induced myogenic constriction was unaffected. Chronic treatment with raloxifene restored ACh-induced dilatation in cholesterol-fed Ovx hamsters. U46619-induced constriction was increased in arteries from cholesterol-fed Ovx hamsters but not from cholesterol-fed control hamsters, which was normalized by chronic raloxifene treatment. The pressure-diameter relationship is presented as normalized diameter versus intraluminal pressure, while the effect of ACh or U46619 is expressed as percentage of tone at 80 mmHg. Two-way analysis of variance (ANOVA) followed by Bonferroni post-tests were used for statistical evaluation among different treatment groups. P < 0.05 was taken as statistically significant. The present results show that chronic treatment with raloxifene could benefit myogenically active coronary arteries by (i) restoring ACh-induced dilatation and (ii) reducing U46619-induced constriction without affecting pressure-induced myogenic responses in cholesterol-fed hamsters during estrogen deficiency. If such benefit can be observed in humans, raloxifene and other SERMs may be useful to preserve endothelial function and curtail vascular hypersensitivity in resistance coronary arteries in post-menopausal women with hypercholesterolemia or hyperlipidemia, a lipid condition implicated in the pathogenesis of myocardial infarction. © 2011 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/134638
ISSN
2015 Impact Factor: 4.816
2015 SCImago Journal Rankings: 2.108
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong Kong4362/04M
National Basic Research Program of China2012CB517805
CUHK
Funding Information:

This study was supported by Research Grants Council of Hong Kong (4362/04M), National Basic Research Program of China (2012CB517805) and CUHK Focused Investment Scheme.

References

 

DC FieldValueLanguage
dc.contributor.authorChan, YCen_HK
dc.contributor.authorLeung, FPen_HK
dc.contributor.authorTian, XYen_HK
dc.contributor.authorYung, LMen_HK
dc.contributor.authorLau, CWen_HK
dc.contributor.authorChen, ZYen_HK
dc.contributor.authorYao, Xen_HK
dc.contributor.authorLaher, Ien_HK
dc.contributor.authorHuang, Yen_HK
dc.date.accessioned2011-07-05T01:44:13Z-
dc.date.available2011-07-05T01:44:13Z-
dc.date.issued2012en_HK
dc.identifier.citationPharmacological Research, 2012, v. 65 n. 2, p. 182-188en_HK
dc.identifier.issn1043-6618en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134638-
dc.description.abstractAlthough vascular effects of selective estrogen receptor modulators (SERMs) have been extensively examined in conduit arteries, whether SERMs could favorably modulate myogenic response in resistance arteries is unknown. The impact of raloxifene therapy and cholesterol diet on myogenic constriction during estrogen deficiency is unresolved. This study investigated changes in vascular reactivity and myogenic responses in female ovariectomized (Ovx) hamsters fed high-cholesterol diet (HCD) with and without chronic treatment of raloxifene. Functional studies were performed on hamster septal coronary arteries cannulated in a pressure myograph. Acetylcholine (ACh)-induced dilatation was reduced in arteries from cholesterol-fed Ovx hamsters, but not in those from cholesterol-fed hamsters, while pressure-induced myogenic constriction was unaffected. Chronic treatment with raloxifene restored ACh-induced dilatation in cholesterol-fed Ovx hamsters. U46619-induced constriction was increased in arteries from cholesterol-fed Ovx hamsters but not from cholesterol-fed control hamsters, which was normalized by chronic raloxifene treatment. The pressure-diameter relationship is presented as normalized diameter versus intraluminal pressure, while the effect of ACh or U46619 is expressed as percentage of tone at 80 mmHg. Two-way analysis of variance (ANOVA) followed by Bonferroni post-tests were used for statistical evaluation among different treatment groups. P < 0.05 was taken as statistically significant. The present results show that chronic treatment with raloxifene could benefit myogenically active coronary arteries by (i) restoring ACh-induced dilatation and (ii) reducing U46619-induced constriction without affecting pressure-induced myogenic responses in cholesterol-fed hamsters during estrogen deficiency. If such benefit can be observed in humans, raloxifene and other SERMs may be useful to preserve endothelial function and curtail vascular hypersensitivity in resistance coronary arteries in post-menopausal women with hypercholesterolemia or hyperlipidemia, a lipid condition implicated in the pathogenesis of myocardial infarction. © 2011 Elsevier Ltd. All rights reserved.en_HK
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618en_HK
dc.relation.ispartofPharmacological Researchen_HK
dc.subjectCholesterolen_HK
dc.subjectHamsteren_HK
dc.subjectMyogenic constrictionen_HK
dc.subjectOvariectomyen_HK
dc.subjectRaloxifeneen_HK
dc.subjectSeptal coronary arteriesen_HK
dc.titleRaloxifene improves vascular reactivity in pressurized septal coronary arteries of ovariectomized hamsters fed cholesterol dieten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1043-6618&volume=&spage=&epage=&date=2010&atitle=Raloxifene+improves+vascular+reactivity+in+pressurized+septal+coronary+arteries+of+ovariectomized+hamsters+fed+cholesterol+diet-
dc.identifier.emailChan, YC:yauchi@graduate.hku.hken_HK
dc.identifier.authorityChan, YC=rp01502en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.phrs.2011.09.010en_HK
dc.identifier.pmid22005391-
dc.identifier.scopuseid_2-s2.0-84856019163en_HK
dc.identifier.hkuros174015-
dc.identifier.hkuros203417-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856019163&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume65en_HK
dc.identifier.issue2en_HK
dc.identifier.spage182en_HK
dc.identifier.epage188en_HK
dc.identifier.isiWOS:000301868300005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, YC=7403676116en_HK
dc.identifier.scopusauthoridLeung, FP=8615375300en_HK
dc.identifier.scopusauthoridTian, XY=35768379500en_HK
dc.identifier.scopusauthoridYung, LM=13807768200en_HK
dc.identifier.scopusauthoridLau, CW=7401968520en_HK
dc.identifier.scopusauthoridChen, ZY=53663102300en_HK
dc.identifier.scopusauthoridYao, X=7402529434en_HK
dc.identifier.scopusauthoridLaher, I=7005431686en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.citeulike9910938-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats