C242T polymorphism of the NADPH oxidase p22PHOX gene and its association with endothelial dysfunction in asymptomatic individuals with essential systemic hypertension.

Vascular oxidative stress is an important factor in hypertension-associated vascular damage and is mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation. The C242T polymorphism at the p22PHOX gene affects binding of p22PHOX to heme, leading to variants of NADPH oxidase that produce different levels of reactive oxygen species (ROS). Specific variations in ROS are associated with an altered risk of developing cardiovascular disease. In the present study, 140 permanent Kashmiri-resident individuals were recruited (75 with essential systemic hypertension and 65 normotensive controls). Endothelial function was assessed non-invasively using high-resolution ultrasonography of the brachial artery. Endothelium-dependent vasoreactivity was expressed in terms of flow-mediated dilation. The TT genotype was identified in 2% of hypertensive and 7% of normotensive individuals. Frequency of the T-allele was not observed as significantly different between hypertensive and normotensive individuals (P=0.24; OR=0.4; 95% CI, 0.07-2.2). Blood pressure or the prevalence of hypertension did not vary between C242T p22PHOX genotypes or in the presence or absence of the T-allele.