The XXXX p22phox polymorphism and endothelium-dependent vasodilation in subjects with hypercholesterolaemia.

@entity1 @entity1115 @entity26884 @entity1854 @entity1110 @entity7293 @entity842 @entity453 @entity224 @entity65 @entity165 @entity934
Oxidative stress plays a major pathogenetic role in @entity65 . The @entity26884 variant of the @entity1115 gene encoding the p22phox subunit of the @entity1110 oxidase, a major source of @entity224 production, has been shown to be associated with @entity453 and with vascular @entity224 production in @entity1 veins ex vivo. Since @entity224 degrades @entity842 (NO), we hypothesized that the @entity26884 variant influences endothelium-dependent vasodilation of the @entity1 forearm vasculature in vivo. In the present study, 90 subjects with elevated @entity165 levels were stratified for the @entity26884 polymorphism of the @entity1115 p22phox gene. Endothelium-dependent and -independent vasodilation were assessed by plethysmographic monitoring of forearm blood flow responses to intra-arterial infusion of @entity934 and @entity1854 respectively. @entity7293 ( @entity7293 ) was infused to analyse NO-mediated basal vascular tone. Baseline parameters (age, gender, blood pressure, body mass index, @entity165 level) were similar across the genotypes. No differences in forearm blood flow responses to the intra-arterial infusion of @entity934 , @entity1854 or @entity7293 were found across the @entity1115 p22phox genotypes. Our sample size of n =90 had a power of >80% (beta=0.20) with a P value of <0.05 (alpha=0.05) to detect a difference greater than 156% in the forearm blood flow response to @entity934 across genotypes (S.D. 336%; average increase in forearm blood flow=514%). In conclusion, at a power of 80%, our study excludes a major effect of the @entity26884 @entity1115 p22phox polymorphism on @entity934 -mediated endothelium-dependent vasodilation and basal NO-mediated vascular tone of the @entity1 forearm circulation in subjects with hypercholesterolaemia.
