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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-8-25
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1522-1490
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R723-8
pubmed:dateRevised
2010-9-2
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Pressure-induced constriction is inhibited in a mouse model of reduced betaENaC.
pubmed:affiliation
Dept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural