Linked Life Data

14989558

Source:http://linkedlifedata.com/resource/pubmed/id/14989558

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-3-1
pubmed:abstractText
The products of nitric oxide synthase (NOS) and angiotensin-converting enzyme (ACE) play a critical role in determining vessel wall structure and function. Polymorphisms in both genes have been independently demonstrated to influence propensity to cardiovascular events. The purpose of this study was to determine the influence of the homozygous G849T (Glu298-->Asp) polymorphism in NOS III on peripheral conduit artery endothelial function and to elucidate the modifier role, if any, of a common ACE polymorphism. Three hundred and ninety-seven consecutive subjects presenting to the cardiac catheterization laboratory of the University of Michigan over a period of 18 months were recruited. DNA was extracted and polymerase chain reaction (PCR) analysis for ACE and NOS polymorphisms performed. Patients with homozygosity for G849T at both loci (TT) who belong to DD and II ACE genotype (groups 1 and 2) and those who are negative for this polymorphism (GG) and belong to either DD or II genotype (groups 3 and 4) were identified. The four groups then underwent determination of conduit endothelial function. Heterozygosity of Glu298-Asp or the ID variant of the ACE were not studied. Median FMD value in the TT-DD group was 0.20 (-3.17, 2.01) compared with 2.23% (-0.29, 4.17) in the GG-II group. Median values in the TT-II and the GG-DD groups were 3.04 (-1.16, 6.61) and 2.46% (-1.83, 6.52) respectively. These values were not statistically significant (p > 0.05 by one-way ANOVA). Median nitroglycerin-mediated dilation in the four groups did not differ between the four groups (p = NS by ANOVA). Atherosclerosis burdens as assessed by angiography were not different across the groups. In conclusion, the homozygous NOS III variant (GG) status does not seem to interact additively with the ACE homozygous DD genotype in determining flow-mediated vasodilation in individuals with established atherosclerosis and pre-existent endothelial dysfunction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1358-863X
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-83
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:14989558-Aged, pubmed-meshheading:14989558-Brachial Artery, pubmed-meshheading:14989558-Coronary Artery Disease, pubmed-meshheading:14989558-DNA, pubmed-meshheading:14989558-DNA Primers, pubmed-meshheading:14989558-Endothelium, Vascular, pubmed-meshheading:14989558-Female, pubmed-meshheading:14989558-Genetic Predisposition to Disease, pubmed-meshheading:14989558-Homozygote, pubmed-meshheading:14989558-Humans, pubmed-meshheading:14989558-Male, pubmed-meshheading:14989558-Middle Aged, pubmed-meshheading:14989558-Nitric Oxide Synthase, pubmed-meshheading:14989558-Nitric Oxide Synthase Type III, pubmed-meshheading:14989558-Polymerase Chain Reaction, pubmed-meshheading:14989558-Polymorphism, Genetic, pubmed-meshheading:14989558-Renin, pubmed-meshheading:14989558-Vasodilation
pubmed:year
2003
pubmed:articleTitle
Interactive effects of the ACE DD polymorphism with the NOS III homozygous G849T (Glu298-->Asp) variant in determining endothelial function in coronary artery disease.
pubmed:affiliation
Section of Vascular Medicine, Division of Cardiology, University of Michigan School of Medicine, Ann Arbor, MI 48109-0273, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't