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Involvement of the renin–angiotensin system in the development of vascular damage in a rat model of arthritis: Effect of angiotensin receptor blockers

dc.contributor.authorSakuta, Takeoen_US
dc.contributor.authorMorita, Yoshitakaen_US
dc.contributor.authorSatoh, Minoruen_US
dc.contributor.authorFox, David A.en_US
dc.contributor.authorKashihara, Naokien_US
dc.date.accessioned2010-06-02T19:49:34Z
dc.date.available2011-03-01T16:26:43Zen_US
dc.date.issued2010-05en_US
dc.identifier.citationSakuta, Takeo; Morita, Yoshitaka; Satoh, Minoru; Fox, David A.; Kashihara, Naoki (2010). "Involvement of the renin–angiotensin system in the development of vascular damage in a rat model of arthritis: Effect of angiotensin receptor blockers." Arthritis & Rheumatism 62(5): 1319-1328. <http://hdl.handle.net/2027.42/75773>en_US
dc.identifier.issn0004-3591en_US
dc.identifier.issn1529-0131en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/75773
dc.description.abstractObjective To explore the involvement of the renin–angiotensin system (RAS) in the development of vascular damage in adjuvant-induced arthritis (AIA) in rats. Methods Angiotensin II (Ang II; 0.25 or 1.0 mg/kg/day) was infused in control rats and rats with AIA for 21 days, and the impact of systemic inflammation on Ang II–induced hypertension, endothelial dysfunction, and vascular hypertrophy was evaluated. Expression of angiotensin II type 1 receptor (AT 1 R) and angiotensin-converting enzyme (ACE) in the aortas of rats with AIA were examined by real-time polymerase chain reaction (PCR) and Western blot analyses. Losartan (3 mg/kg/day) or irbesartan (5 mg/kg/day), both of which are AT 1 R blockers, was administered orally to rats with AIA for 21 days. In situ superoxide production in aortas was assessed according to the fluorogenic oxidation of dihydroethidium to ethidium. The expression and activity of NAD(P)H oxidases in aortas were examined by real-time PCR analysis and lucigenin chemiluminescence assay. Endothelial function in rats with AIA treated in vivo or ex vivo with AT 1 R blockers was also determined. Results The Ang II–induced hypertensive response, endothelial dysfunction, and vascular hypertrophy were exacerbated in rats with AIA. Expression of AT 1 R and ACE was increased in the aortas of rats with AIA. Both losartan and irbesartan decreased the levels of superoxide and the expression and activity NAD(P)H oxidases in the aortas of rats with AIA. The endothelial dysfunction in AIA was improved by the in vivo or ex vivo treatment with AT 1 R blockers. Conclusion The locally activated RAS is involved in the increased vascular oxidative stress and endothelial dysfunction in AIA. Our findings have important implications for clinical approaches to the reduction of cardiovascular risk in patients with rheumatoid arthritis.en_US
dc.format.extent231857 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.titleInvolvement of the renin–angiotensin system in the development of vascular damage in a rat model of arthritis: Effect of angiotensin receptor blockersen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelGeriatricsen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumUniversity of Michigan, Ann Arboren_US
dc.contributor.affiliationotherKawasaki Medical School, Kurashiki, Japanen_US
dc.contributor.affiliationotherKawasaki Medical School, Kurashiki, Japan ; Drs. Morita and Satoh contributed equally to this work. ; Department of Rheumatology, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japanen_US
dc.contributor.affiliationotherKawasaki Medical School, Kurashiki, Japanen_US
dc.contributor.affiliationotherKawasaki Medical School, Kurashiki, Japanen_US
dc.identifier.pmid20213806en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/75773/1/27384_ftp.pdf
dc.identifier.doi10.1002/art.27384en_US
dc.identifier.sourceArthritis & Rheumatismen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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