Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-5-24
pubmed:abstractText
Arterial stiffness is a moderately heritable trait that is affected by alterations in the bioavailability of NO. Previous studies have found associations between variants in the gene for endothelial NO synthase (NOS3) and arterial properties. We previously identified a linkage peak for forward pressure wave amplitude in the immediate vicinity of NOS3. Therefore, we evaluated relations between arterial stiffness measures and common genetic variants at this locus. Eighteen single nucleotide polymorphisms capturing approximately 90% of underlying common variation in NOS3 were genotyped in unrelated Framingham Heart Study participants (N=1157; 52.2% women; mean age: 62 years) with routinely ascertained tonometry data that provided 5 arterial phenotypes (forward and reflected pressure wave amplitude, central pulse pressure, carotid-femoral pulse wave velocity, and mean arterial pressure). In women but not men, the genotype for the common NOS3 missense mutation (Glu298Asp, rs1799983) was related to central pulse pressure (women: GG=53+/-0.9, GT=54+/-0.9, and TT=47+/-2.0 mm Hg, P=0.0047; men: GG=50+/-1.0, GT=49+/-0.9, and TT=47+/-1.8 mm Hg, P=0.30) and forward wave amplitude (women: GG=41+/-0.7, GT=42+/-0.7, and TT=38+/-1.6 mm Hg, P=0.029; men: GG=42+/-0.9, GT=41+/-0.8, and TT=39+/-1.5 mm Hg, P=0.47). The only other nominally significant sex-specific association in men but not women was between an intronic polymorphism (rs1800781) and reflected wave amplitude (women: AA=10.4+/-0.4, AG=11.1+/-0.6, and GG=8.9+/-2.2 mm Hg, P=0.50; men: AA=6.1+/-0.3, AG=7.3+/-0.5, and GG=11.3+/-2.3 mm Hg, P=0.014). After adjusting for multiple testing (18 polymorphisms and 5 phenotypes), these nominal associations were no longer significant. The present study was suggestive of modest relations between common genetic variants at the NOS3 locus and arterial stiffness.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1285-90
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17404185-Aged, pubmed-meshheading:17404185-Arteries, pubmed-meshheading:17404185-Atherosclerosis, pubmed-meshheading:17404185-Blood Pressure, pubmed-meshheading:17404185-Carotid Arteries, pubmed-meshheading:17404185-Cohort Studies, pubmed-meshheading:17404185-Elasticity, pubmed-meshheading:17404185-Female, pubmed-meshheading:17404185-Femoral Artery, pubmed-meshheading:17404185-Genetic Linkage, pubmed-meshheading:17404185-Genotype, pubmed-meshheading:17404185-Humans, pubmed-meshheading:17404185-Male, pubmed-meshheading:17404185-Middle Aged, pubmed-meshheading:17404185-Mutation, Missense, pubmed-meshheading:17404185-Nitric Oxide Synthase Type III, pubmed-meshheading:17404185-Phenotype, pubmed-meshheading:17404185-Polymorphism, Single Nucleotide, pubmed-meshheading:17404185-Pulsatile Flow, pubmed-meshheading:17404185-Regional Blood Flow, pubmed-meshheading:17404185-Sex Factors
pubmed:year
2007
pubmed:articleTitle
Vascular stiffness and genetic variation at the endothelial nitric oxide synthase locus: the Framingham Heart study.
pubmed:affiliation
Cardiovascular Engineering, Inc., Waltham, MA 02453, USA. GaryFMitchell@mindspring.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural