| Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats. | |
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MedLine Citation:
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PMID: 19648216 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Abnormalities 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. |
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Authors:
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O G??kalp; S Ozdem; S D??nmez; M Dogan; H Demirin; H Y Kara; R S??tc??; E Cicek; M K Ozer; N Delibas |
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Publication Detail:
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Type: Journal Article Date: 2009-07-31 |
Journal Detail:
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Title: Toxicology and industrial health Volume: 25 ISSN: 0748-2337 ISO Abbreviation: Toxicol Ind Health Publication Date: 2009 Aug |
Date Detail:
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Created Date: 2009-09-28 Completed Date: 2010-01-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8602702 Medline TA: Toxicol Ind Health Country: England |
Other Details:
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Languages: eng Pagination: 447-53 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, School of Medicine, Dicle University, Diyarbakir, Turkey. ogokalp@med.sdu.edu.tr |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Animals Arginine / pharmacology Cadmium / toxicity* Endothelium, Vascular / physiopathology* Hypertension / chemically induced*, physiopathology* Male Malondialdehyde / blood NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / blood Nitroprusside / pharmacology Rats Vasodilation / drug effects*, physiology |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 542-78-9/Malondialdehyde; 74-79-3/Arginine; 7440-43-9/Cadmium |
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