Vasoconstrictor responses after neo-intima formation and endothelial removal in the rabbit carotid artery

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dc.contributor.authorDe Meyer G.R.Y.
dc.contributor.authorBult H.
dc.contributor.authorÜstünes L.
dc.contributor.authorKockx M.
dc.contributor.authorJordaens F.H.
dc.contributor.authorZonnekeyn L.L.
dc.contributor.authorHerman A.G.
dc.date.accessioned2019-10-27T00:33:52Z
dc.date.available2019-10-27T00:33:52Z
dc.date.issued1994
dc.departmentEge Üniversitesien_US
dc.description.abstractThe present study examined the responses of the rabbit carotid artery to five vasoconstrictors after neo-intima formation induced by perivascular collar treatment and evaluated the role of constitutive and inducible nitric oxide (NO) synthase and endothelial cells (ECs). Ring segments of the rabbit carotid artery were mounted in organ chambers for isometric tension recording. Neo-intima-bearing vessels developed less force (Emax) in response to KCl, the thromboxanemimetic U-46619 and 5-hydroxytryptamine (5-HT), but not to angiotensin I and II. The collar-treatment increased the sensitivity to 5-HT, and decreased the sensitivity to angiotensin II. The sensitivity to U-46619 and angiotensin I remained unchanged. Mechanical removal of ECs and inhibition of NO biosynthesis by NG-monomethyl-l-arginine (l-NMMA) and NG-nitro-l-arginine (l-NOARG) increased the sensitivity to 5-HT in sham and collar-treated segments to the same extent. The effects of collar-treatment and endothelial removal or treatment with inhibitors of NO biosynthesis were additive. Inhibition of NO biosynthesis failed to augment sensitivity to 5-HT after endothelial denudation. l-NOARG increased the force development to KCl in sham and collar-treated segments to the same extent. However, l-NMMA and l-NOARG failed to augment the contractile responses of neo-intima-bearing vessels to 5-HT and KCl after endothelial removal. The responses to angiotensin I were not altered, either by the neo-intima or by endothelial removal. In arteries with a neo-intima the sensitivity to angiotensin II was decreased. Removal of the endothelium or incubation with l-NOARG counteracted this rightward shift and increased Emax. Our results demonstrate that contractions to 5-HT, angiotensin II and KCl are modulated by NO in both sham and neo-intima-bearing vessels. Inhibition of NO biosynthesis and collar treatment resulted in additive effects on the EC50 values, suggesting that the 5-HT and angiotensin (AT) receptors on the smooth muscle cells are also modified by the formation of a neo-intima. Furthermore, the reduced contractile responses of segments with a neo-intima are not due to NO formed by an inducible NO synthase in those vessels. 1994 British Pharmacological Societyen_US
dc.identifier.doi10.1111/j.1476-5381.1994.tb13097.xen_US
dc.identifier.endpage476en_US
dc.identifier.issn0007-1188
dc.identifier.issue2en_US
dc.identifier.pmid7521257en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage471en_US
dc.identifier.urihttps://doi.org/10.1111/j.1476-5381.1994.tb13097.x
dc.identifier.urihttps://hdl.handle.net/11454/24145
dc.identifier.volume112en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subject5-HTen_US
dc.subjectangiotensinen_US
dc.subjectendotheliumen_US
dc.subjectinducible nitric oxide synthase (iNOS)en_US
dc.subjectneo-intimaen_US
dc.subjectNitric oxideen_US
dc.subjectpotassium chlorideen_US
dc.subjectsilicone collaren_US
dc.subjectU-46619en_US
dc.titleVasoconstrictor responses after neo-intima formation and endothelial removal in the rabbit carotid arteryen_US
dc.typeArticleen_US

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