What you carry at this position in your DNA and what research says about it.
Heart and Vascular Health: 7/10 evidence, 62 publications.
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Sample genotype (not yours): G/G
Typical Nitric Oxide Levels and Normal Vascular Risk
Normal levels of the eNOS enzyme and typical nitric oxide production characterize this genotype. It does not elevate the risk for cardiovascular conditions, preeclampsia, or stroke.
What this genotype means: Typical nitric oxide production; Standard baseline risk for cardiovascular disease; Standard response to vascular medications.
Sample genotype (not yours): T/G
Slightly Reduced Nitric Oxide and Mildly Elevated Vascular Risk
A single copy of the T allele is linked to a slight reduction in nitric oxide availability. This may mildly increase the risk of preeclampsia during pregnancy and affect responses to certain heart medications.
What this genotype means: Slightly lower nitric oxide availability; Mildly increased risk of preeclampsia; Slightly higher risk of stent re-narrowing with antiplatelets.
Sample genotype (not yours): T/T
Reduced Nitric Oxide and Elevated Cardiovascular Risk
Double copies of the T allele are associated with lower nitric oxide production and reduced vascular elasticity. This increases the risk of ischemic heart disease, stroke, and preeclampsia.
What this genotype means: Lower nitric oxide production; Increased risk of ischemic heart disease and stroke; Elevated risk of preeclampsia during pregnancy.
Gene function and biological role
Gene Function: The NOS3 gene encodes endothelial nitric oxide synthase (eNOS), an enzyme responsible for producing nitric oxide in the lining of blood vessels [1]. Nitric oxide is a crucial signaling molecule that regulates vascular tone, promotes blood vessel dilation, and inhibits platelet aggregation [2]. Proper eNOS function is essential for maintaining healthy blood pressure and preventing cardiovascular diseases [3]. Reduced activity of this enzyme can lead to endothelial dysfunction, which is a key early step in the development of atherosclerosis [4].
Variant Impact: The rs1799983 variant, also known as Glu298Asp, is a missense mutation in exon 7 of the NOS3 gene [3]. This genetic change replaces the amino acid glutamate with aspartate at position 298 of the enzyme [5]. The aspartate-encoding T allele is reported to undergo selective proteolysis, which reduces the overall availability of the eNOS enzyme in endothelial cells [2]. Consequently, individuals carrying the T allele may have lower nitric oxide production, potentially affecting blood vessel relaxation and increasing susceptibility to vascular complications [1].
Key Insight: The T allele of this variant undergoes selective cellular breakdown, leading to lower levels of the nitric oxide-producing enzyme. This can influence how blood vessels respond to dietary fats and certain cardiovascular medications.
Location: NOS3. Chromosome 7 · 7q36.1 · 151.0 Mb
Estimated prevalence by population
Global 6.9%; European 10.9%; African 1.3%; East Asian 1.3%; South Asian 3.2%; Americas 6.6%; Ashkenazi 3.7%; Finnish 8.7%; Middle Eastern 6.9%; Amish 5.4%.
Estimated TT genotype frequency.
Global 35.1%; European 44.3%; African 20.2%; East Asian 19.9%; South Asian 29.4%; Americas 38.1%; Ashkenazi 31.2%; Finnish 41.5%; Middle Eastern 38.7%; Amish 35.7%.
Estimated TG genotype frequency.
Global 58.0%; European 44.8%; African 78.6%; East Asian 78.8%; South Asian 67.4%; Americas 55.4%; Ashkenazi 65.1%; Finnish 49.8%; Middle Eastern 54.5%; Amish 58.8%.
Estimated GG genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Heart Disease
Coronary Artery Disease. Evidence: 4/10. Source: PMID 10510054. Typical Risk.
Stroke
Stroke. Evidence: 7/10. Source: PMID 30383316. Typical Risk.
Endocrine & Reproductive
Pregnancy & Birth Complications
Preeclampsia. Evidence: 4/10. Source: PMID 23333443. Typical Risk.
Pharmacogenomics
Cardiovascular Drug Response
Vascular Medication Risk. Evidence: 5/10. Source: PMID 22543981. Typical Response.
Showing effects for T/G genotype
Stroke. Evidence: 7/10. Source: PMID 30383316. Slightly Increased.
Preeclampsia. Evidence: 4/10. Source: PMID 23333443. Slightly Increased.
Vascular Medication Risk. Evidence: 5/10. Source: PMID 22543981. Slightly Higher Risk.
Showing effects for T/T genotype
Coronary Artery Disease. Evidence: 4/10. Source: PMID 10510054. ~1.3x Increased Risk.
Stroke. Evidence: 7/10. Source: PMID 30383316. ~1.1x Increased Risk.
Preeclampsia. Evidence: 4/10. Source: PMID 23333443. Increased Risk.
Vascular Medication Risk. Evidence: 5/10. Source: PMID 22543981. Higher Risk of Events.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Production of the typical, fully functional form of the endothelial nitric oxide synthase enzyme occurs with this genotype [1]. This enzyme maintains healthy blood vessel dilation and blood flow by producing adequate amounts of nitric oxide [2]. Clinical databases classify this genotype as benign, indicating it does not elevate the risk for essential hypertension, preeclampsia, or coronary artery spasm [3]. Studies show that individuals with this genotype have a typical baseline risk for ischemic heart disease and stroke [4]. Additionally, when undergoing cardiovascular treatments or procedures like stenting, those with this genotype show a standard response to common medications like beta-blockers and aspirin [2]. This standard response helps avoid the increased risk of stent re-narrowing seen in other genotypes [2]. Maintaining a balanced diet and regular exercise further supports healthy vascular function. Overall, this genotype represents the most common and low-risk genetic profile for nitric oxide production.
Typical nitric oxide production; Standard baseline risk for cardiovascular disease; Standard response to vascular medications.
Sample genotype: TG (Heterozygous)
Inheriting one copy of the T allele means a portion of the eNOS enzymes produced contain aspartate instead of glutamate, which can slightly reduce overall nitric oxide production [1]. This mild reduction in vascular nitric oxide is associated with an increased susceptibility to preeclampsia during pregnancy [2]. Research also indicates a slightly higher risk of stent re-narrowing after coronary procedures when taking antiplatelet therapies like aspirin or clopidogrel [3]. However, the risk for major cardiovascular events like ischemic heart disease is generally not as pronounced as in those with two copies of the T allele [4]. This genotype represents an intermediate state where maintaining a heart-healthy lifestyle is beneficial for vascular function [3]. Regular physical activity can help stimulate nitric oxide production through other pathways. Monitoring blood pressure during pregnancy is a common precautionary measure for individuals with this profile. Overall, cardiovascular risks remain only mildly elevated compared to the baseline population.
Slightly lower nitric oxide availability; Mildly increased risk of preeclampsia; Slightly higher risk of stent re-narrowing with antiplatelets.
Sample genotype: TT (Homozygous)
Two copies of the T allele lead to a significant reduction in active eNOS enzymes because the aspartate-containing variant is more prone to cellular breakdown [1]. This reduction in enzyme availability leads to lower nitric oxide levels, which can impair the ability of blood vessels to dilate properly [2]. Large-scale meta-analyses have linked this genotype to an increased risk of ischemic heart disease, with some studies showing an odds ratio of approximately 1.31 [3]. It is also associated with a higher risk of stroke and white matter hyperintensities in the brain [4]. During pregnancy, this genotype significantly elevates the risk of developing preeclampsia [5]. Furthermore, individuals with this genotype may have an increased risk of adverse outcomes or emergency visits when taking certain cardiovascular medications like beta-blockers [6].
Lower nitric oxide production; Increased risk of ischemic heart disease and stroke; Elevated risk of preeclampsia during pregnancy; Altered response to beta-blockers and other heart medications.
Variants with shared genetic architecture
rs3918226 · NOS3 Gene · Chr 7 · Cardiovascular Risk
rs891511 · NOS3 Gene · Chr 7 · Blood Pressure
rs2070744 · NOS3 Gene · Chr 7 · Heart and Vascular Health
Genome-wide meta-analysis identifies 3 novel loci associated with stroke.
Pharmacogenetics and healthcare outcomes in patients with chronic heart failure.
Content updated August 2026.
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