Posttransplantation Therapeutic Rapamycin Concentration Protects Nitric Oxide-Related Vascular Endothelial Function: Comparative Effects in Rat Thoracic Aorta and Coronary Endothelial Cell Culture

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dc.contributor.authorParlar, A.
dc.contributor.authorCan, C.
dc.contributor.authorErol, A.
dc.contributor.authorUlker, S.
dc.date.accessioned2019-10-27T21:17:38Z
dc.date.available2019-10-27T21:17:38Z
dc.date.issued2010
dc.departmentEge Üniversitesien_US
dc.description.abstractObjective. To investigate the potential effects of therapeutic dosages of the immunosuppression agent rapamycin on endothelial function with regard to nitric oxide (NO) synthesis in rat thoracic aorta in vivo and rat coronary endothelial cells in vitro. Materials and Methods. Male Wistar rats were injected with rapamycin, 1.5 mg/kg/d intraperitoneally for 14 days. After the rats were sacrificed, the thoracic aortas were suspended in organ chambers and evaluated for endothelium-dependent and endothelium-independent vascular responses. Results. Rapamycin administration resulted in increased relaxant responses to L-arginine and to greater concentrations of the calcium ionophore (A23187) in the aortas. However, potassium chloride, acetylcholine, sodium nitroprusside, and N-G-nitro-L-arginine methyl ester responses remained unchanged. In addition, phenylephrine-induced contractions were significantly decreased in the aortas regardless of the presence of functional endothelium. In a series of in vitro experiments, isolated rat coronary endothelial cells were incubated with therapeutic concentrations of rapamycin (10 nmol/L). Nitrite accumulation in the supernatants revealed that rapamycin decreased nitrite release induced by interleukin-1 beta but did not affect basal or A23187-stimulated nitrite levels. Western blot analysis demonstrated that rapamycin decreased inducible NO synthase protein expression in coronary endothelial cells. Conclusion. Posttransplantation therapeutic concentrations of rapamycin not only preserve vascular endothelial function mediated by NO synthesis but possibly interact in vivo with adrenergic receptors in favor of vasodilatory mechanisms.en_US
dc.description.sponsorshipEge University Research FoundationEge University; Bayindir Hospitals, Turkeyen_US
dc.description.sponsorshipThis study was supported by the Ege University Research Foundation and by Bayindir Hospitals Medical Research Project Award 2005, Bayindir Hospitals, Turkey.en_US
dc.identifier.doi10.1016/j.transproceed.2010.03.134en_US
dc.identifier.endpage1930en_US
dc.identifier.issn0041-1345
dc.identifier.issn1873-2623
dc.identifier.issue5en_US
dc.identifier.pmid20620549en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage1923en_US
dc.identifier.urihttps://doi.org/10.1016/j.transproceed.2010.03.134
dc.identifier.urihttps://hdl.handle.net/11454/43850
dc.identifier.volume42en_US
dc.identifier.wosWOS:000279236100108en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofTransplantation Proceedingsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.titlePosttransplantation Therapeutic Rapamycin Concentration Protects Nitric Oxide-Related Vascular Endothelial Function: Comparative Effects in Rat Thoracic Aorta and Coronary Endothelial Cell Cultureen_US
dc.typeArticleen_US

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