These results indicate that somatic delivery of the human eNOS gene induces a prolonged reduction of high blood pressure and raises the potential of using eNOS gene therapy for hypertension and cardiovascular diseases.
Since NOS-III is also expressed in vascular cells, and cerebrovascular disease (CVD) frequently complicates the pathology of AD, we investigated the role of NOS-III in relation to CVD in AD.
Surprisingly, only approximately half of these studies have demonstrated significant associations between NOS3 polymorphisms and cardiovascular disease, and many reports are contradictory.
The marked interethnic differences that we found in the distribution of eNOS variants, in the estimated haplotype frequency, and in the association between variants may help us to understand how the combination of these genetic variants may influence cardiovascular diseases.
An insertion/deletion (I/D) polymorphism in the gene encoding the ACE and a single nucleotide exchange polymorphism (G894T) in the gene NOS3 encoding endothelial nitric oxide synthase have been associated with cardiovascular disorders.
We sought to determine whether the endothelial nitric oxide synthase (eNOS) T-786C single nucleotide polymorphism (SNP), implicated in cardiovascular disease susceptibility, could facilitate differentiation between small (< or =5 mm) versus large (> or =10 mm) ruptured aneurysms.
Several polymorphisms of the gene encoding ENOS are now known and have been investigated with respect to their influence on cardiovascular disease risk in the general population.
Our results imply that G894T polymorphism of the endothelial nitric oxide synthase gene is associated with elevated levels of inflammatory and oxidative stress markers, which may partially explain the increased prevalence of G894T polymorphism among patients with cardiovascular disease.
Our results imply that G894T polymorphism of the endothelial nitric oxide synthase gene is associated with elevated levels of inflammatory and oxidative stress markers, which may partially explain the increased prevalence of G894T polymorphism among patients with cardiovascular disease.
The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.
The current studies offer a new paradigm in which to study the non-cholesterol effects of SR-BI, HDL, and eNOS on the development of atherosclerosis and potentially other cardiovascular diseases.
Genetic variation of the RAS and NOS3 genes do not appear to strongly influence subclinical cardiovascular disease or blood pressure in this diabetic population.
An interaction between the E298D and T-786C polymorphisms in NOS3, cigarette smoking, and risk of incident coronary heart disease and ischemic stroke events appears to exist, suggesting a potential complex interplay between genetic and environmental factors and cardiovascular disease risk.
In this study, associations between CVDs and polymorphisms of angiotensin-converting enzyme (ACE), atrial natriuretic peptide (ANP), beta(2)-adrenal receptor (B2AR) and endothelial nitric oxide synthase (ENOS) genes were explored in a community-based setting.
Clear is that enhanced production of reactive oxygen species (ROS) and eNOS uncoupling are relatively important causes of reduced NO-bioactivity in cardiovascular disease states.
Specifically, polymorphisms of the endothelial nitric oxide synthase gene (eNOS) have been reported to be associated with multiple health conditions including DR, hypertension, nephropathy, and cardiovascular diseases in several ethnic groups.
The eNOS gene has a number of polymorphic sites, including SNPs, dinucleotide repeats and variable number tandem repeat sequences, and the opportunity exists to investigate polymorphic functional correlates as well as disease-specific associations, especially in cardiovascular disease, including coronary artery disease, and its most severe consequence, myocardial infarction.