Genetic variation of the RAS and NOS3 genes do not appear to strongly influence subclinical cardiovascular disease or blood pressure in this diabetic population.
However, the genetic background may also affect NO formation in the cardiovascular system, and recent studies have shown that genetic polymorphisms in the eNOS gene modify endogenous NO formation and the risk of developing cardiovascular diseases.
However, we found that eNOSG894T polymorphism was associated with the presence and severity of renal disease and with CVD in CRD patients (P=0.028, P=0.018, P=0.016 respectively).
Impaired endothelial function, characterized by an imbalance in endothelial Nitric Oxide Synthase (eNOS) activity, precedes and accelerates the development of CVD.
In this review, we discuss the basic biochemical mechanisms of NOS3 regulation and the clinical and pharmacogenetic impact of NOS3 polymorphisms on cardiovascular diseases.
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.
It was postulated that Hg exposure might decrease circulating nitrite concentrations and that variants in the eNOS gene might enhance the adverse effects of Hg resulting in increased risk of cardiovascular disease.
Loss of endothelial BH<sub>4</sub> is observed in cardiovascular disease (CVD) states and results in decreased NO and increased superoxide (O<sub>2</sub><sup>-</sup>) generation via eNOS uncoupling.
Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling).
NO is synthesized from l-arginine through the action of the nitric oxide synthase (NOS) family of enzymes, which includes three isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). iNOS-derived NO has been associated with the pathogenesis and progression of several diseases, including liver diseases, insulin resistance, obesity and diseases of the cardiovascular system.
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.
Presence of endothelial nitric oxide synthase (eNOS) gene polymorphism has been associated with cardiovascular disease (CVD) whereas exercise training (EX) promotes beneficial effects on CVD which is related to increased nitric oxide levels (NO).
Several polymorphisms in the eNOS gene have been described, some of them being linked with the increased risk of cardiovascular disease, coronary heart disease (CHD), and coronary spasm.
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.
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.
Some studies have reported a possible relationship between endothelial nitric oxide synthase (eNOS) and metabolic syndrome (MS), which is associated with an increased risk for cardiovascular disease.
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.
Surprisingly, only approximately half of these studies have demonstrated significant associations between NOS3 polymorphisms and cardiovascular disease, and many reports are contradictory.