Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

种族/民族决定了心血管疾病高风险人群中氧化应激标志物与血压之间的关系

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作者:G Kapuku, F Treiber, F Raouane, J Halbert, H Davis, S Young-Mayes, V Robinson, G Harshfield

Abstract

Oxidative stress (OS) and cardiovascular (CV) reactivity are related to CV morbidity and mortality. However, little is known about the relationships between these CV risk factors and their confounders. We hypothesize that higher OS is linked to higher blood pressure (BP) reactivity to acute laboratory stressors and in the natural setting. We studied 137 subjects with a family history of hypertension and early myocardial infarction. There were 63 European Americans (EAs) (38 males) and 74 African Americans (AAs) (35 males), aged 19-36 (27.6±3.1). The protocol included a competitive video game, cold stressor and ambulatory BP recording. Blood samples were drawn six times for OS markers (8-hydroxydeoxyguanosine (8-OHdG) and 8-Isoprostane) assay. Repeated measures analyses of covariance were used to test for mean differences and Pearson correlations were used to test OS and BP associations. There were no significant race/ethnicity differences in BP reactivity to either stressor (both P's>0.48). 8-OHdG levels were significantly lower across all time points for AAs than for EAs (P<0.05), while levels of 8-isoprostane did not differ significantly (P>0.10). Averaged 8-OHdG levels significantly correlated with systolic blood pressure (SBP) reactivity (r=0.45, <0.01) and 24-h, daytime and nighttime SBP (r range=0.37-0.42, all P's<0.02) for EAs but not for AAs, whereas 8-isoprostane levels were significantly correlated with reactive SBP and nighttime diastolic blood pressure (DBP) (both r's=0.38, P<0.01) for AAs but not for EAs. These findings suggest a link between OS and BP changes in subjects at high risk for CV disease (CVD). Further, race/ethnicity determines which OS marker will impact BP variation implying race/ethnicity differences in OS-related mechanisms of CVD.

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