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Article: Two isoforms of cyclooxygenase contribute to augmented endothelium- dependent contractions in femoral arteries of 1-year-old rats

TitleTwo isoforms of cyclooxygenase contribute to augmented endothelium- dependent contractions in femoral arteries of 1-year-old rats
Authors
KeywordsAging
Cyclooxygenase
Endothelium
Endothelium-dependent contraction
Endothelium-derived contracting factor
Oxidative stress
Reactive oxygen species
Thromboxane-prostanoid receptors
Issue Date2008
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica, 2008, v. 29 n. 2, p. 185-192 How to Cite?
AbstractAim: The present experiments were designed to study the changes in endothelium-dependent contractions with aging. Methods: The rat femoral arteries of 20-week and 1-year-old rats with and without endothelium were suspended in organ chambers to record isometric tension. The production of oxygen-derived free radicals in the endothelium was measured with 2′,7′- dichlorodihydrofluorescein diacetate (DCF) using confocal microscopy. Protein presences were determined by Western blotting. Results: In the arteries from the 1-year-old rats, endothelium-dependent relaxations to A23187 were reduced, but the endothelium-dependent contractions to A23187 (in the presence of N ω-nitro-L-arginine methyl ester hydrochloride [L-NAME; an inhibitor of nitric oxide synthase]) were augmented, demonstrating endothelial dysfunction with aging. Indomethacin normalized the responses, suggesting that a cyclooxygenase (COX)-dependent contraction is prominent in aging. The endothelium-dependent contractions were also prevented by terutroban (a blocker of thromboxane-prostanoid receptors), confirming the activation of thromboxane-prostanoid receptors on vascular smooth muscle. Valeryl salicylate and NS-398 (preferential inhibitors of COX-1 and COX-2, respectively) partially reduced the response, indicating that both COX-1 and COX-2 are involved. Western blotting confirmed the upregulation of both isoforms in the arteries of the 1-year-old rats. In the presence of L-NAME, A23187 increased the DCF fluorescence in the endothelium, demonstrating that the production of oxygen-derived free radicals contributes to endothelium-dependent contractions. The activity of catalase was reduced in the arteries with endothelium of 1-year-old rats, indicating that hydrogen peroxide is the likely mediator of increased oxidative stress in the aging endothelium. Conclusion: Endothelium-dependent contractions are augmented with aging. Oxidative stress potentiates the response, and both COX-1 and COX-2 are involved. © 2008 CPS and SIMM.
Persistent Identifierhttp://hdl.handle.net/10722/80223
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShi, Yen_HK
dc.contributor.authorMan, RYen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:03:54Z-
dc.date.available2010-09-06T08:03:54Z-
dc.date.issued2008en_HK
dc.identifier.citationActa Pharmacologica Sinica, 2008, v. 29 n. 2, p. 185-192en_HK
dc.identifier.issn1671-4083en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80223-
dc.description.abstractAim: The present experiments were designed to study the changes in endothelium-dependent contractions with aging. Methods: The rat femoral arteries of 20-week and 1-year-old rats with and without endothelium were suspended in organ chambers to record isometric tension. The production of oxygen-derived free radicals in the endothelium was measured with 2′,7′- dichlorodihydrofluorescein diacetate (DCF) using confocal microscopy. Protein presences were determined by Western blotting. Results: In the arteries from the 1-year-old rats, endothelium-dependent relaxations to A23187 were reduced, but the endothelium-dependent contractions to A23187 (in the presence of N ω-nitro-L-arginine methyl ester hydrochloride [L-NAME; an inhibitor of nitric oxide synthase]) were augmented, demonstrating endothelial dysfunction with aging. Indomethacin normalized the responses, suggesting that a cyclooxygenase (COX)-dependent contraction is prominent in aging. The endothelium-dependent contractions were also prevented by terutroban (a blocker of thromboxane-prostanoid receptors), confirming the activation of thromboxane-prostanoid receptors on vascular smooth muscle. Valeryl salicylate and NS-398 (preferential inhibitors of COX-1 and COX-2, respectively) partially reduced the response, indicating that both COX-1 and COX-2 are involved. Western blotting confirmed the upregulation of both isoforms in the arteries of the 1-year-old rats. In the presence of L-NAME, A23187 increased the DCF fluorescence in the endothelium, demonstrating that the production of oxygen-derived free radicals contributes to endothelium-dependent contractions. The activity of catalase was reduced in the arteries with endothelium of 1-year-old rats, indicating that hydrogen peroxide is the likely mediator of increased oxidative stress in the aging endothelium. Conclusion: Endothelium-dependent contractions are augmented with aging. Oxidative stress potentiates the response, and both COX-1 and COX-2 are involved. © 2008 CPS and SIMM.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.htmlen_HK
dc.relation.ispartofActa Pharmacologica Sinicaen_HK
dc.subjectAgingen_HK
dc.subjectCyclooxygenaseen_HK
dc.subjectEndotheliumen_HK
dc.subjectEndothelium-dependent contractionen_HK
dc.subjectEndothelium-derived contracting factoren_HK
dc.subjectOxidative stressen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectThromboxane-prostanoid receptorsen_HK
dc.titleTwo isoforms of cyclooxygenase contribute to augmented endothelium- dependent contractions in femoral arteries of 1-year-old ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailMan, RY: rykman@hkucc.hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityMan, RY=rp00236en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1745-7254.2008.00749.xen_HK
dc.identifier.pmid18215347-
dc.identifier.scopuseid_2-s2.0-38749089857en_HK
dc.identifier.hkuros151868en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38749089857&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue2en_HK
dc.identifier.spage185en_HK
dc.identifier.epage192en_HK
dc.identifier.isiWOS:000252805200008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShi, Y=7404964959en_HK
dc.identifier.scopusauthoridMan, RY=7004986435en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike2321548-

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