Source:http://linkedlifedata.com/resource/pubmed/id/19553501
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2009-8-25
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pubmed:abstractText |
Recent studies suggest certain epithelial Na(+) channel (ENaC) proteins may be components of mechanosensitive ion channel complexes in vascular smooth muscle cells that contribute to pressure-induced constriction in middle cerebral arteries (MCA). However, the role of a specific ENaC protein, betaENaC, in pressure-induced constriction of MCAs has not been determined. The goal of this study was to determine whether pressure-induced constriction in the MCA is altered in a mouse model with reduced levels of betaENaC. Using quantitative immunofluorescence, we found whole cell betaENaC labeling in cerebral vascular smooth muscle cells (VSMCs) was suppressed 46% in betaENaC homozygous mutant (m/m) mice compared with wild-type littermates (+/+). MCAs from betaENaC +/+ and m/m mice were isolated and placed in a vessel chamber for myographic analysis. Arteries from betaENaC+/+ mice constricted to stepwise increases in perfusion pressure and developed maximal tone of 10 +/- 2% at 90 mmHg (n = 5). In contrast, MCAs from betaENaC m/m mice developed significantly less tone (4 +/- 1% at 90 mmHg, n = 5). Vasoconstrictor responses to KCl (4-80 mM) were identical between genotypes and responses to phenylephrine (10(-7)-10(-4) M) were marginally altered, suggesting that reduced levels of VSMC betaENaC specifically inhibit pressure-induced constriction. Our findings indicate betaENaC is required for normal pressure-induced constriction in the MCA and provide further support for the hypothesis that betaENaC proteins are components of a mechanosensor in VSMCs.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epithelial Sodium Channel,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Scnn1b protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1522-1490
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
297
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R723-8
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pubmed:dateRevised |
2010-9-2
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pubmed:meshHeading |
pubmed-meshheading:19553501-Animals,
pubmed-meshheading:19553501-Blood Pressure,
pubmed-meshheading:19553501-Dose-Response Relationship, Drug,
pubmed-meshheading:19553501-Down-Regulation,
pubmed-meshheading:19553501-Epithelial Sodium Channel,
pubmed-meshheading:19553501-Mechanotransduction, Cellular,
pubmed-meshheading:19553501-Mice,
pubmed-meshheading:19553501-Mice, Mutant Strains,
pubmed-meshheading:19553501-Middle Cerebral Artery,
pubmed-meshheading:19553501-Muscle, Smooth, Vascular,
pubmed-meshheading:19553501-Mutation,
pubmed-meshheading:19553501-Phenylephrine,
pubmed-meshheading:19553501-Potassium Chloride,
pubmed-meshheading:19553501-Vasoconstriction,
pubmed-meshheading:19553501-Vasoconstrictor Agents
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pubmed:year |
2009
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pubmed:articleTitle |
Pressure-induced constriction is inhibited in a mouse model of reduced betaENaC.
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pubmed:affiliation |
Dept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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