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The aim of our study was to investigate the putative direct pro\u2010inflammatory and vasomotor effects of Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>and compare to those of lipopolysaccharides (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>) in mouse isolated mesenteric resistance\u2010sized arteries (<jats:styled-content style=\"fixed-case\">MRA<\/jats:styled-content>) supported by experiments in cultured human primary endothelial and vascular smooth muscle cells. Results showed that 24\u2010hr organ culture of mouse<jats:styled-content style=\"fixed-case\">MRA<\/jats:styled-content>with 10 nM Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>had, unlike 100 ng\/mL<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>, no effects on<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 or<jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\u20101 secretion,<jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>1<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>expression or endothelial function, while Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>significantly decreased maximal vasomotor responses to phenylephrine. In support, 24\u2010hr organ culture of mouse<jats:styled-content style=\"fixed-case\">MRA<\/jats:styled-content>significantly suppressed Agtr1a<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>and augmented Tlr4<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>along with attenuated vasomotor responses to Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>. Moreover, contrary to<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>and [Sar1]\u2010Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>had no concentration\u2010 or time\u2010dependent effects on<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106 and<jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\u20101 secretion in human umbilical vein endothelial cells (<jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>) and human aortic smooth muscle cells (<jats:styled-content style=\"fixed-case\">HASMC<\/jats:styled-content>).<jats:styled-content style=\"fixed-case\">AGTR<\/jats:styled-content>1 or<jats:styled-content style=\"fixed-case\">AGTR<\/jats:styled-content>2<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>expression was undetectable in<jats:styled-content style=\"fixed-case\">HUVEC<\/jats:styled-content>, whereas<jats:styled-content style=\"fixed-case\">HASMC<\/jats:styled-content>expressed only<jats:styled-content style=\"fixed-case\">AGTR<\/jats:styled-content>1<jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>. In summary, contrary to previous studies and the observed effects of<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>, we could not demonstrate direct vascular pro\u2010inflammatory effects of Ang<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content><jats:italic>ex vivo<\/jats:italic>or<jats:italic>in vitro<\/jats:italic>. As indicated by our results, down\u2010regulation or desensitization of<jats:styled-content style=\"fixed-case\">AT<\/jats:styled-content><jats:sub>1<\/jats:sub>R during culture may explain our findings.<\/jats:p>","DOI":"10.1111\/bcpt.12697","type":"journal-article","created":{"date-parts":[[2016,11,4]],"date-time":"2016-11-04T08:19:37Z","timestamp":1478247577000},"page":"335-347","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Lipopolysaccharides, but not Angiotensin ll, lnduces Direct Pro\u2010lnflammatory Effects in Cultured Mouse Arteries and Human Endothelial and Vascular Smooth Muscle Cells"],"prefix":"10.1111","volume":"120","author":[{"given":"Emilie M.","family":"Outzen","sequence":"first","affiliation":[{"name":"Department of Drug Design and Pharmacology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marina","family":"Zaki","sequence":"additional","affiliation":[{"name":"Department of Drug Design and Pharmacology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rahila","family":"Mehryar","sequence":"additional","affiliation":[{"name":"Department of Drug Design and Pharmacology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bahareh","family":"Abdolalizadeh","sequence":"additional","affiliation":[{"name":"Department of Drug Design and Pharmacology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Waseem","family":"Sajid","sequence":"additional","affiliation":[{"name":"Department of Diabetes Complications Biology Novo Nordisk A\/S Maaloev Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harrie C. 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