Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats

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dc.contributor.authorGokalp, O.
dc.contributor.authorOzdem, S.
dc.contributor.authorDonmez, S.
dc.contributor.authorDogan, M.
dc.contributor.authorDemirin, H.
dc.contributor.authorKara, H. Y.
dc.contributor.authorSutcu, R.
dc.date.accessioned2024-04-24T17:14:35Z
dc.date.available2024-04-24T17:14:35Z
dc.date.issued2009
dc.departmentDicle Üniversitesien_US
dc.description.abstractAbnormalities in the production and/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg/kg/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10(-9)-10(-4) M) and sodium nitroprusside (SNP, 10(-10)-10(-5) M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N-G-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10(-3) M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.en_US
dc.identifier.doi10.1177/0748233709106822
dc.identifier.endpage453en_US
dc.identifier.issn0748-2337
dc.identifier.issn1477-0393
dc.identifier.issue7en_US
dc.identifier.pmid19648216
dc.identifier.scopus2-s2.0-70349479414
dc.identifier.scopusqualityQ2
dc.identifier.startpage447en_US
dc.identifier.urihttps://doi.org/10.1177/0748233709106822
dc.identifier.urihttps://hdl.handle.net/11468/18078
dc.identifier.volume25en_US
dc.identifier.wosWOS:000270194600002
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherSage Publications Incen_US
dc.relation.ispartofToxicology and Industrial Health
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAcetylcholineen_US
dc.subjectCadmiumen_US
dc.subjectHypertensionen_US
dc.subjectMalondialdehydeen_US
dc.subjectNitric Oxideen_US
dc.titleImpairment of endothelium-dependent vasorelaxation in cadmium-hypertensive ratsen_US
dc.titleImpairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats
dc.typeArticleen_US

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