Linked Life Data

18296560

Source:http://linkedlifedata.com/resource/pubmed/id/18296560

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2008-4-2
pubmed:abstractText
Recent studies from our laboratory demonstrated the importance of mechanosensitive epithelial Na(+) channel (ENaC) proteins in pressure-induced constriction in renal and cerebral arteries. ENaC proteins are closely related to acid-sensing ion channel 2 (ASIC2), a protein known to be required for normal mechanotransduction in certain sensory neurons. However, the role of the ASIC2 protein in pressure-induced constriction has never been addressed. The goal of the current study was to investigate the role of ASIC2 proteins in pressure-induced, or myogenic, constriction in the mouse middle cerebral arteries (MCAs) from ASIC2 wild-type (+/+), heterozygous (+/-), and null (-/-) mice. Constrictor responses to KCl (20-80 mM) and phenylephrine (10(-7)-10(-4) M) were not different among groups. However, vasoconstrictor responses to increases in intraluminal pressure (15-90 mmHg) were impaired in MCAs from ASIC2(-/-) and (+/-) mice. At 60 and 90 mmHg, MCAs from ASIC2(+/+) mice generated 13.7 +/- 2.1% and 15.8 +/- 2.0% tone and ASIC2(-/-) mice generated 7.4 +/- 2.8% and 12.5 +/- 2.4% tone, respectively. Surprisingly, MCAs from ASIC2(+/-) mice generated 1.2 +/- 2.2% and 3.9 +/- 1.8% tone at 60 and 90 mmHg. The reason underlying the total loss of myogenic tone in the ASIC2(+/-) is not clear, although the loss of mechanosensitive beta- and gamma-ENaC proteins may be a contributing factor. These results demonstrate that normal ASIC2 expression is required for normal pressure-induced constriction in the MCA. Furthermore, ASIC2 may be involved in establishing the basal level of myogenic tone.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
294
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1793-803
pubmed:meshHeading
pubmed-meshheading:18296560-Animals, pubmed-meshheading:18296560-Dose-Response Relationship, Drug, pubmed-meshheading:18296560-Epithelial Sodium Channel, pubmed-meshheading:18296560-Female, pubmed-meshheading:18296560-Genotype, pubmed-meshheading:18296560-Male, pubmed-meshheading:18296560-Mechanotransduction, Cellular, pubmed-meshheading:18296560-Membrane Proteins, pubmed-meshheading:18296560-Mice, pubmed-meshheading:18296560-Mice, Knockout, pubmed-meshheading:18296560-Middle Cerebral Artery, pubmed-meshheading:18296560-Muscle, Smooth, Vascular, pubmed-meshheading:18296560-Nerve Tissue Proteins, pubmed-meshheading:18296560-Phenotype, pubmed-meshheading:18296560-Phenylephrine, pubmed-meshheading:18296560-Potassium Chloride, pubmed-meshheading:18296560-Pressure, pubmed-meshheading:18296560-Protein Isoforms, pubmed-meshheading:18296560-Protein Subunits, pubmed-meshheading:18296560-Sodium Channels, pubmed-meshheading:18296560-Vasoconstriction, pubmed-meshheading:18296560-Vasoconstrictor Agents
pubmed:year
2008
pubmed:articleTitle
Impaired pressure-induced constriction in mouse middle cerebral arteries of ASIC2 knockout mice.
pubmed:affiliation
Dept. of Physiology and Biophysics, Univesity of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural