Source:http://linkedlifedata.com/resource/pubmed/id/15637112
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2005-4-20
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pubmed:abstractText |
The role of mitochondrial manganese-superoxide dismutase (Mn-SOD) in the maintenance of vascular function has not yet been studied. Thus we examined flow- and agonist-induced dilations in isolated mesenteric arteries (approximately 90 microm in diameter) of Mn-SOD heterozygous (Mn-SOD+/-) and wild-type (WT) mice. Increases in flow elicited dilations in all vessels, but the magnitude of the dilation was significantly less in vessels of Mn-SOD+/- mice than in those of WT mice (64 vs. 74% of passive diameter). N(omega)-nitro-L-arginine methyl ester inhibited the dilation in vessels of WT mice but had no effect on vessels of Mn-SOD+/- mice. Tempol or tiron (superoxide scavengers) increased flow-induced dilation in vessels of Mn-SOD+/- mice. Acetylcholine- and sodium nitroprusside-induced, but not adenosine-induced, dilations were also decreased in arteries of Mn-SOD+/- mice. Superoxide levels in the arteries of Mn-SOD+/- mice were significantly increased. Western blot analysis confirmed a 50% reduction of Mn-SOD protein in the vessels of Mn-SOD+/- mice. A 41% reduction in endothelial nitric oxide synthase (eNOS) protein and a 37% reduction in eNOS activity were also found in the vessels of Mn-SOD+/- mice. Whereas there was no difference in eNOS protein in kidney homogenates of WT and Mn-SOD+/- mice, a significant reduction of nitric oxide synthase activity was found in Mn-SOD+/- mice, which could be restored by the administration of tiron. We conclude that an increased concentration of superoxide due to reduced activity of Mn-SOD, which inactivates nitric oxide and inhibits eNOS activity, contributes to the impaired vasodilator function of isolated mesenteric arteries of Mn-SOD+/- mice. These results suggest that Mn-SOD contributes significantly to the regulation of vascular function.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/HL-31069,
http://linkedlifedata.com/resource/pubmed/grant/HL-50412,
http://linkedlifedata.com/resource/pubmed/grant/HL-68813,
http://linkedlifedata.com/resource/pubmed/grant/HL-70653,
http://linkedlifedata.com/resource/pubmed/grant/P0-1-HL-43203,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL070653-01A1,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL070653-02
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
288
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H2225-31
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pubmed:dateRevised |
2011-11-1
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pubmed:meshHeading |
pubmed-meshheading:15637112-Animals,
pubmed-meshheading:15637112-Endothelium, Vascular,
pubmed-meshheading:15637112-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:15637112-Male,
pubmed-meshheading:15637112-Mesenteric Arteries,
pubmed-meshheading:15637112-Mice,
pubmed-meshheading:15637112-Mice, Mutant Strains,
pubmed-meshheading:15637112-Nitric Oxide Synthase,
pubmed-meshheading:15637112-Nitric Oxide Synthase Type II,
pubmed-meshheading:15637112-Nitric Oxide Synthase Type III,
pubmed-meshheading:15637112-Regional Blood Flow,
pubmed-meshheading:15637112-Stress, Mechanical,
pubmed-meshheading:15637112-Superoxide Dismutase,
pubmed-meshheading:15637112-Superoxides,
pubmed-meshheading:15637112-Vasodilation,
pubmed-meshheading:15637112-Vasodilator Agents
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pubmed:year |
2005
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pubmed:articleTitle |
Increased superoxide leads to decreased flow-induced dilation in resistance arteries of Mn-SOD-deficient mice.
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pubmed:affiliation |
Deptartment of Physiology, New York Medical College, Valhalla, New York 10595, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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