Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7908
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dc.contributor.authorManicam, Caroline-
dc.contributor.authorStaubitz, Julia-
dc.contributor.authorBrochhausen, Christoph-
dc.contributor.authorGrus, Franz-Hermann-
dc.contributor.authorPfeiffer, Norbert-
dc.contributor.authorGericke, Adrian-
dc.date.accessioned2022-10-07T09:38:41Z-
dc.date.available2022-10-07T09:38:41Z-
dc.date.issued2016
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/7923-
dc.description.abstractCholinergic regulation of arterial luminal diameter involves intricate network of intercellular communication between the endothelial and smooth muscle cells that is highly dependent on the molecular mediators released by the endothelium. Albeit the well-recognized contribution of nitric oxide (NO) towards vasodilation, the identity of compensatory mechanisms that maintain vasomotor tone when NO synthesis is deranged remain largely unknown in the ophthalmic artery. This is the first study to identify the vasodilatory signalling mechanisms of the ophthalmic artery employing wild type mice. Acetylcholine (ACh)-induced vasodilation was only partially attenuated when NO synthesis was inhibited. Intriguingly, the combined blocking of cytochrome P450 oxygenase (CYP450) and lipoxygenase (LOX), as well as CYP450 and gap junctions, abolished vasodilation; demonstrating that the key compensatory mechanisms comprise arachidonic acid metabolites which, work in concert with gap junctions for downstream signal transmission. Furthermore, the voltage-gated potassium ion channel, Kv1.6, was functionally relevant in mediating vasodilation. Its localization was found exclusively in the smooth muscle. In conclusion, ACh-induced vasodilation of mouse ophthalmic artery is mediated in part by NO and predominantly via arachidonic acid metabolites, with active involvement of gap junctions. Particularly, the Kv1.6 channel represents an attractive therapeutic target in ophthalmopathologies when NO synthesis is compromised.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.titleThe gatekeepers in the mouse ophthalmic artery: endothelium-dependent mechanisms of cholinergic vasodilationen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-7908-
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.volume6de
jgu.pages.alternativeArt. 20322de
jgu.publisher.year2016-
jgu.publisher.nameNature Publishing Groupde
jgu.publisher.placeLondonde
jgu.publisher.urihttp://dx.doi.org/10.1038/srep20322de
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
opus.date.modified2018-08-23T08:01:13Z
opus.subject.dfgcode00-000
opus.organisation.stringFB 04: Medizin: Institut für Pathologiede_DE
opus.organisation.stringFB 04: Medizin: Augenklinik und Poliklinikde_DE
opus.identifier.opusid56279
opus.institute.number0423
opus.institute.number0446
opus.metadataonlyfalse
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_EN
opus.affiliatedBrochhausen, Christoph
opus.affiliatedGrus, Franz-Hermann
opus.affiliatedPfeiffer, Norbert
opus.affiliatedGericke, Adrian
jgu.publisher.doi10.1038/srep20322de
jgu.organisation.rorhttps://ror.org/023b0x485-
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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