Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7153
Full metadata record
DC FieldValueLanguage
dc.contributor.authorManicam, Caroline-
dc.contributor.authorGinter, Natalja-
dc.contributor.authorLi, Huige-
dc.contributor.authorXia, Ning-
dc.contributor.authorGoloborodko, Evgeny-
dc.contributor.authorZadeh, Jenia Kouchek-
dc.contributor.authorMusayeva, Aytan-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorGericke, Adrian-
dc.date.accessioned2022-06-15T08:25:22Z-
dc.date.available2022-06-15T08:25:22Z-
dc.date.issued2017
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7167-
dc.description.abstractNitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays an important role in the maintenance of ocular vascular homeostasis. Therefore, perturbations in vascular NO synthesis have been implicated in the pathogenesis of several ocular diseases. We recently reported that eNOS contributes significantly to vasodilation of the mouse ophthalmic artery. Interestingly, dilatory responses were also retained in eNOS gene-deficient mice (eNOS−/−), indicating inherent endothelial adaptive mechanism(s) that act as back-up systems in chronic absence of eNOS to preserve vasorelaxation. Thus, this study endeavoured to identify the compensatory mechanism(s) in the ophthalmic artery of eNOS−/− mice employing isolated arterial segments and pharmacological inhibitors in vitro. Endothelium removal virtually abolished acetylcholine (ACh)-induced vasodilation, suggesting an obligatory involvement of the endothelium in cholinergic control of vascular tone. However, non-NOS and non-cyclooxygenase components compensate for eNOS deficiency via endothelium-derived hyperpolarizing factors (EDHFs). Notably, arachidonic acid-derived metabolites of the 12-lipoxygenase pathway were key mediators in activating the inwardly rectifying potassium channels to compensate for chronic lack of eNOS. Conclusively, endothelium-dependent cholinergic responses of the ophthalmic artery in the eNOS−/− mice are largely preserved and, this vascular bed has the ability to compensate for the loss of normal vasodilator responses solely via EDHFs.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizinde
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleCompensatory vasodilator mechanisms in the ophthalmic artery of endothelial nitric oxide synthase gene knockout miceen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7153-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleScientific reportsde
jgu.journal.volume7de
jgu.pages.alternativeArt. 7111de
jgu.publisher.year2017-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttp://dx.doi.org/10.1038/s41598-017-07768-7de
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-03-15T11:30:58Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Institut für Pharmakologiede_DE
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid57978
opus.institute.number0413
opus.institute.number0446
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedLi, Huige
opus.affiliatedXia, Ning
opus.affiliatedPfeiffer, Norbert
opus.affiliatedGericke, Adrian
jgu.publisher.doi10.1038/s41598-017-07768-7de
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

Files in This Item:
  File Description SizeFormat
Thumbnail
compensatory_vasodilator_mech-20220612163724820.pdf1.8 MBAdobe PDFView/Open