Modulation of Vasodilator Response via the Nitric Oxide Pathway after Acute Methyl Mercury Chloride Exposure in Rats

dc.contributor.authorOmanwar, S
dc.contributor.authorB, Saidullah
dc.contributor.authorK, Ravi
dc.contributor.authorM, Fahim
dc.date.accessioned2017-07-06T10:47:17Z
dc.date.available2017-07-06T10:47:17Z
dc.date.copyright2013en_US
dc.description.abstractMercury exposure induces endothelial dysfunction leading to loss of endothelium-dependent vasorelaxation due to decreased nitric oxide (NO) bioavailability via increased oxidative stress. Our aim was to investigate whether acute treatment with methyl mercury chloride changes the endothelium-dependent vasodilator response and to explore the possible mechanisms behind the observed effects. Wistar rats were treated with methyl mercury chloride (5 mg/kg, po.). The methyl mercury chloride treatment resulted in an increased aortic vasorelaxant response to acetylcholine (ACh). In methyl-mercury-chloride-exposed rats, the % change in vasorelaxant response of ACh in presence of Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME;  M) was significantly increased, and in presence of glybenclamide ( M), the response was similar to that of untreated rats, indicating the involvement of NO and not of endothelium-derived hyperpolarizing factor (EDHF). In addition, superoxide dismutase (SOD) + catalase treatment increased the NO modulation of vasodilator response in methyl-mercury-chloride-exposed rats. Our results demonstrate an increase in the vascular reactivity to ACh in aorta of rats acutely exposed to methyl mercury chloride. Methyl mercury chloride induces nitric oxide synthase (NOS) and increases the NO production along with inducing oxidative stress without affecting the EDHF pathway.en_US
dc.description.searchVisibilitytrueen_US
dc.description.urihttps://www.hindawi.com/journals/bmri/2013/530603/en_US
dc.format.mimetypeapplication/pdfen_US
dc.identifier.urihttps://www.hindawi.com/journals/bmri/2013/530603/en_US
dc.identifier.urihttp://www.ignou.ndl.iitkgp.ac.in:8080/xmlui/handle/123456789/56
dc.language.isoengen_US
dc.publisherHindawi Ltd., Adam Houseen_US
dc.publisher.date2013
dc.publisher.placeLondonen_US
dc.relation.requiresPDF viewer Pluginen_US
dc.rights.accessRightsndlen_US
dc.sourceIGNOUen_US
dc.source.urihttp://www.ignou.ac.in/en_US
dc.subjectEducationen_US
dc.subject.ddc573en_US
dc.subject.otherEducationen_US
dc.titleModulation of Vasodilator Response via the Nitric Oxide Pathway after Acute Methyl Mercury Chloride Exposure in Ratsen_US
dc.typetexten_US
lrmi.educationalAlignment.difficultyLevelmediumen_US
lrmi.educationalAlignment.educationalFrameworkUniversity Grants Commission (UGC)en_US
lrmi.educationalAlignment.educationalLevelug_pgen_US
lrmi.educationalAlignment.pedagogicObjectiveFor Academic and research useen_US
lrmi.educationalRoleteacheren_US
lrmi.educationalUseresearchen_US
lrmi.interactivityTypemixeden_US
lrmi.learningResourceTypearticleen_US
lrmi.typicalAgeRange22+en_US
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