The role of eNOS on the compensatory regulation of vascular tonus by H2S in mouse carotid arteries

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dc.contributor.authorErtuna, Elif
dc.contributor.authorLoot, Annemarieke E.
dc.contributor.authorFleming, Ingrid
dc.contributor.authorYetik-Anacak, Gunay
dc.date.accessioned2019-10-27T11:05:28Z
dc.date.available2019-10-27T11:05:28Z
dc.date.issued2017
dc.departmentEge Üniversitesien_US
dc.description.abstractThe gasotransmitter nitric oxide (NO) has an important role in vascular function and a decrease in its bioavailability is accepted as a main pathological mechanism for cardiovascular diseases. However, other gasotransmitters such as hydrogen sulfide (H2S) are also generated by the endothelium and can also affect vascular tone and a crosstalk may exist between H2S and NO. We therefore investigated the consequences of deficiency, replacement or overexpression of endothelial nitric oxide synthase (eNOS) on H2S-induced vascular responses in murine carotid arteries. In pre-contracted carotid arteries from wild-type (WT) mice, L-cysteine elicited relaxation that was inhibited by the H2S synthesis inhibitor amino-oxyacetic acid (AOAA). Genetic deletion of eNOS increased L-cysteine-induced relaxation compared to WT, but the replacement of eNOS by adenoviral transfection or H2S synthesis inhibition by AOAA reversed it. Furthermore, eNOS deletion did not alter NaHS-induced relaxation in carotid arteries while eNOS overexpression/replacement increased NaHS-induced relaxation responses in carotid arteries from WT or eNOS(-/-). We suggest that, endogenously produced H2S can compensate for impaired vasodilatory responses in the absence of NO to maintain vascular patency; while, eNOS abundance can limit endogenous H2S-induced vascular responses in mice carotid arteries. Our result suggests that endogenous vs. exogenous H2S-induced relaxation are reciprocally regulated by NO in mice carotid arteries. (C) 2017 Elsevier Inc. All rights reserved.en_US
dc.description.sponsorshipTUBITAK (The Scientific and Technological Research Council of Turkey)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [109s453]; STSMen_US
dc.description.sponsorshipThis study was supported by TUBITAK (The Scientific and Technological Research Council of Turkey) grant # 109s453 (GYA) allowing to joining COST action BM1005. The MC members (GYA and IF) thank COST action BM1005 for networking and the support by a STSM (EE).en_US
dc.identifier.doi10.1016/j.niox.2017.04.007en_US
dc.identifier.endpage50en_US
dc.identifier.issn1089-8603
dc.identifier.issn1089-8611
dc.identifier.pmid28414104en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage45en_US
dc.identifier.urihttps://doi.org/10.1016/j.niox.2017.04.007
dc.identifier.urihttps://hdl.handle.net/11454/31678
dc.identifier.volume69en_US
dc.identifier.wosWOS:000408396500006en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAcademic Press Inc Elsevier Scienceen_US
dc.relation.ispartofNitric Oxide-Biology and Chemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjecteNOSen_US
dc.subjectHydrogen sulfideen_US
dc.subjectVascular relaxationen_US
dc.subjectMouse carotid arteryen_US
dc.titleThe role of eNOS on the compensatory regulation of vascular tonus by H2S in mouse carotid arteriesen_US
dc.typeArticleen_US

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