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  • Title: The functional consequence of the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in young healthy volunteers.
    Author: Godfrey V, Chan SL, Cassidy A, Butler R, Choy A, Fardon T, Struthers A, Lang C.
    Journal: Cardiovasc Drug Rev; 2007; 25(3):280-8. PubMed ID: 17919260.
    Abstract:
    OBJECTIVE: To assess the role of the endothelial nitric oxide synthase (eNOS) gene variant as a risk factor for atherosclerosis we sought to investigate whether the Glu298Asp polymorphism of the eNOS gene is associated with functional changes in the endothelium in healthy volunteers. METHODS: Endothelial function was assessed in 68 normal volunteers (ages 18-44 years) by bilateral forearm venous occlusion plethysmography with intraarterial infusions of increasing doses of acetylcholine for endothelial-dependent vasodilation and, with sodium nitroprusside and verapamil for endothelial-independent vasodilation. Blood was genotyped by polymerase chain reaction and BanII digestion. RESULTS: Asp homozygotes (TT) had a decreased vasodilatory response to acetylcholine [forearm blood flow (FBF) ratio between infused and control arm, 2.82 +/- 1.10] when compared to GG variant (FBF ratio to acetylcholine, 3.97 +/- 1.90, p= 0.04) and to a certain extent, the GT variant (FBF ratio to acetylcholine, 3.79 +/- 2.28, p= 0.07). There was no effect of eNOS genotype on the response to the endothelial-independent vasodilators-sodium nitroprusside and verapamil. CONCLUSIONS: Our data show that carriage of the Asp298 variant of the eNOS gene is associated with a blunted endothelial-dependent vasodilation in healthy volunteers. These findings support a genetically determined modulation of endothelial dysfunction, a phenotype of early atherosclerosis in humans.
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