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dc.contributor.authorWright, Will
dc.contributor.authorMacKenzie, Louise Susan
dc.contributor.authorKirkby, N.S.
dc.contributor.authorMitchell, Jane A.
dc.date.accessioned2014-06-24T09:00:40Z
dc.date.available2014-06-24T09:00:40Z
dc.date.issued2013-04
dc.identifier.citationWright , W , MacKenzie , L S , Kirkby , N S & Mitchell , J A 2013 , ' Nitric oxide-dependent vasodilation is compromised in isolated pulmonary arteries from COX knockout mice ' , FASEB Journal , vol. 27 , lb603 .
dc.identifier.issn0892-6638
dc.identifier.otherPURE: 7162039
dc.identifier.otherPURE UUID: a4d0f115-bc73-47c3-8555-9fec00fcf8ca
dc.identifier.urihttp://hdl.handle.net/2299/13786
dc.description.abstractCyclooxygenase (COX) has two isoforms and is essential for prostanoid synthesis. COX-1 is constitutive whilst COX-2 is induced in inflammation. Two COX products, prostacyclin (PGI2) and thromboxane (TxA2), regulate vessel tone; PGI2 mediates vasodilation and platelet inhibition, and TxA2 opposes this. PGI2 therapies are used in pulmonary arterial hypertension (PAH). Endogenous TxA2/PGI2 has been linked to PAH in animal models, but the mechanism and isoform involved is debated. We hypothesized that pulmonary artery (PA) from COX-1–/– and COX-2–/– mice would have altered vasodilatory function compared with wild-type (WT; C57Bl6) mice. Vasomotor responses to contractile and relaxant agents were measured by myography. PA from all mice responded similarly to contraction by high potassium or the TxA2 mimetic, U46619. Relaxation to PGI2 receptor or PPARβ/ agonists was also similar in all PAs. However, COX-1–/– and, to a lesser extent, COX-2–/– PA had impaired vasodilation to acetylcholine (ACh), which stimulates endothelial nitric oxide (NO) release, and COX-1–/– PA also dilated less to sodium nitroprusside (SNP); an NO donor that works on smooth muscle (Fig 1). These data indicate an interaction between COX and NO sensing pathways in pulmonary vessels, and have implications for our understanding of PAH.en
dc.format.extent1
dc.language.isoeng
dc.relation.ispartofFASEB Journal
dc.titleNitric oxide-dependent vasodilation is compromised in isolated pulmonary arteries from COX knockout miceen
dc.contributor.institutionSchool of Life and Medical Sciences
dc.contributor.institutionHealth & Human Sciences Research Institute
dc.contributor.institutionDepartment of Human and Environmental Sciences
dc.contributor.institutionPharmacology and Clinical Science Research
dc.contributor.institutionAgriculture, Food and Veterinary Sciences
dc.contributor.institutionCardiovascular Pathologies
dc.contributor.institutionDiabetic neuropathies
dc.description.statusNon peer reviewed
rioxxterms.versionAM
rioxxterms.typeOther


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