Modulation of Vasodilator Response via the Nitric Oxide Pathway after Acute Methyl Mercury Chloride Exposure in Rats.
Mercury 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-dependen...
| Publicado en: | BioMed Research International Vol. 2013; pp. 530603 - 530604 |
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| Autores principales: | , , , |
| Formato: | Journal Article |
| Publicado: |
Wiley-Blackwell
2013
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=104094547&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 104094547 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 23146133 FT2T jtl: BioMed Research International issn: 23146133 maglogo: N pubinfo: dt: 2013 vid: 2013 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 104094547 2012258996 NLM24024199 PMC3760274 104094547 ppf: 530603 ppct: 1 formats: fmt: @attributes: type: P tig: atl: Modulation of Vasodilator Response via the Nitric Oxide Pathway after Acute Methyl Mercury Chloride Exposure in Rats. aug: au: Omanwar, S Saidullah, B Ravi, K Fahim, M affil: School of Sciences, Indira Gandhi National Open University, New Delhi 110068, India. sug: subj: Acetylcholine Administration and Dosage Organic Chemicals Administration and Dosage Nitric Oxide Metabolism Vasodilator Agents Administration and Dosage Animals Biological Availability Biological Factors Metabolism Lipid Peroxidation Drug Effects Malondialdehyde Metabolism Metabolic Networks and Pathways Drug Effects Oxidoreductases Metabolism Tissue Culture Techniques Oxidative Stress Drug Effects Rats Vasodilation Drug Effects ab: Mercury 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 Nw-Nitro-L-arginine methyl ester hydrochloride (L-NAME; 10-4 M) was significantly increased, and in presence of glybenclamide (10-5 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. pubtype: Academic Journal doctype: Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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