NOS3 is the gene that codes for endothelial nitric oxide synthase (eNOS), a member of the nitric oxide synthase enzyme family. eNOS produces nitric oxide in blood vessel lining cells; nitric oxide is a small signaling molecule that affects vessel relaxation, local blood flow, and interactions between the vessel wall and circulating blood. Several common single nucleotide polymorphisms (SNPs) in NOS3 have been studied for their functional effects and population-level associations. Examples include a promoter variant (rs2070744) and a coding variant (rs1799983, Glu298Asp); research has examined how these and other SNPs relate to NOS3 expression, enzyme stability, and markers of endothelial function. These genetic variants do not determine outcomes alone but help explain individual differences in vascular signaling pathways.

Variants linked with higher predicted NOS3 expression or activity are often described as showing stronger nitric oxide signaling. In that context, a genetic pattern suggesting higher NOS3 activity can be associated with markers consistent with better endothelial-mediated vessel relaxation and related physiological patterns. Conversely, variants associated with lower predicted NOS3 expression or activity may be linked with reduced nitric oxide signaling and related shifts in endothelial markers. Interpretation of any single variant or inferred activity level is most accurate when viewed alongside Cardio Zoomer biomarker results—such as arginine/ADMA balance, oxidative stress, inflammatory markers, and lipid profiles—to reveal the full physiological picture.

Cardio Zoomer reports NOS3 variants to add genetic context to measures of endothelial function and nitric oxide signaling. These SNPs help explain why an individual may show particular patterns in vascular biomarkers, blood flow regulation, or interactions with inflammation and oxidative stress, supporting more personalized assessment of cardiovascular physiology.