Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/123579
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dc.contributor.authorNg, H.en
dc.contributor.authorJelinic, M.en
dc.contributor.authorParry, L.en
dc.contributor.authorLeo, C.en
dc.date.issued2015en
dc.identifier.citationAmerican Journal of Physiology - Heart and Circulatory Physiology, 2015; 309(2):H285-H296en
dc.identifier.issn0363-6135en
dc.identifier.issn1522-1539en
dc.identifier.urihttp://hdl.handle.net/2440/123579-
dc.description.abstractThe vascular effects of exogenous relaxin (Rln) treatment are well established and include decreased myogenic reactivity and enhanced relaxation responses to vasodilators in small resistance arteries. These vascular responses are reduced in older animals, suggesting that Rln is less effective in mediating arterial function with aging. The present study investigated the role of endogenous Rln in the aorta and the possibility that vascular dysfunction occurs more rapidly with aging in Rln-deficient (Rln(-/-)) mice. We compared vascular function and underlying vasodilatory pathways in the aorta of male wild-type (Rln(+/+)) and Rln(-/-) mice at 4 and 16 mo of age using wire myography. Superoxide production, but not nitrotyrosine or NADPH oxidase expression, was significantly increased in the aorta of young Rln(-/-) mice, whereas endothelial nitric oxide (NO) synthase and basal NO availability were both significantly decreased compared with Rln(+/+) mice. In the presence of the cyclooxygenase inhibitor indomethacin, sensitivity to ACh was significantly decreased in young Rln(-/-) mice, demonstrating altered NO-mediated relaxation that was normalized in the presence of a membrane-permeable SOD or ROS scavenger. These vascular phenotypes were not exacerbated in old Rln(-/-) mice and, in most cases, did not differ significantly from old Rln(+/+) mice. Despite the vascular phenotypes in Rln(-/-) mice, endothelium-dependent and -independent vasodilation were not adversely affected. Our data show a role for endogenous Rln in reducing superoxide production and maintaining NO availability in the aorta but also demonstrate that Rln deficiency does not compromise vascular function in this artery or exacerbate endothelial dysfunction associated with aging.en
dc.description.statementofresponsibilityHooi H. Ng, Maria Jelinic, Laura J. Parry and Chen-Huei Leoen
dc.language.isoenen
dc.publisherAmerican Physiological Societyen
dc.rights© 2015 the American Physiological Societyen
dc.subjectaorta; endothelium; nitric oxide; relaxin; superoxideen
dc.titleIncreased superoxide production and altered nitric oxide-mediated relaxation in the aorta of young but not old male relaxin-deficient miceen
dc.typeJournal articleen
dc.identifier.rmid1000004909en
dc.identifier.doi10.1152/ajpheart.00786.2014en
dc.relation.granthttp://purl.org/au-research/grants/arc/LP110200543en
dc.identifier.pubid505315-
pubs.library.collectionEnvironment Institute publicationsen
pubs.library.teamDS10en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidParry, L. [0000-0002-6883-3418]en
Appears in Collections:Environment Institute publications

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