Abstract
BackgroundReactive oxygen species are implicated in the physiopathogenesis of salt-induced hypertension and the C242T polymorphism of the p22-phox gene has been associated with higher superoxide production. This study investigated the impact of this polymorphism on the relationship between urinary sodium excretion (USE) and blood pressure levels in an urban Brazilian population.MethodsWe cross-sectionally evaluated 1,298 subjects from the city of Vitoria-ES, located in the Southeast region of Brazil, by clinical history, physical examination, anthropometry, analysis of laboratory parameters, USE measurement and p22-phox C242T polymorphism genotyping.ResultsNo significant differences in studied parameters were detected between the studied genotype groups (CC vs. CT+TT). Systolic blood pressure exhibited significant correlation with USE only in T allele carriers (r = 0.166; p<0.001), while diastolic blood pressure and hypertension status correlated with USE in both genotypes albeit more weakly in subjects with CC genotype (r = 0.098; p = 0.021 and r = 0.105; p = 0.013, respectively) than in T carriers (r = 0.236; p<0.001 and r = 0.213; p<0.001, respectively). Regression analyses adjusted for confounding factors showed that USE remained independently associated with systolic (p<0.001) and diastolic blood pressure (p<0.001) and hypertension status (p = 0.004) only in T allele carriers. Finally, higher diastolic and systolic blood pressure levels were detected in T allele carriers than in CC genotype individuals in the highest tertile of USE.ConclusionsThe p22-phox 242T allele is associated with higher blood pressure levels among subjects with higher USE in an urban Brazilian population.
Highlights
Oxidative stress, exerted by intracellular accumulation of reactive oxygen species, has been implicated in the physiopathogenesis of salt-induced hypertension [1,2]
Bivariate analysis revealed a significant correlation between systolic blood pressure and urinary sodium excretion only in allele T carriers (r = 0.166; p,0.001), while diastolic blood pressure correlated with urinary sodium excretion in both genotype groups, albeit more weakly in CC genotype than in T carriers (CC: r = 0.098; p = 0.021; T carriers: r = 0.236; p,0.001; zscore = 22.54; p = 0.011)
Significant correlation coefficients between hypertension status and urinary sodium excretion were detected in both genotype groups albeit more weakly in CC genotype than in T carriers (CC: r = 0.105; p = 0.011; T carriers: r = 0.213; p,0.001; z-score = 21.98; p = 0.047)
Summary
Oxidative stress, exerted by intracellular accumulation of reactive oxygen species, has been implicated in the physiopathogenesis of salt-induced hypertension [1,2]. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system is a major source of reactive oxygen species and is composed of multiple subunits of membrane and cytosolic components that assemble on the cellular surface to generate reactive oxygen species [3]. Among these subunits the p22-phox is highlighted as an essential membraneassociated factor that plays a crucial role in the activation and stabilization of NADPH oxidase [4]. Reactive oxygen species are implicated in the physiopathogenesis of salt-induced hypertension and the C242T polymorphism of the p22-phox gene has been associated with higher superoxide production. This study investigated the impact of this polymorphism on the relationship between urinary sodium excretion (USE) and blood pressure levels in an urban Brazilian population
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