Hydrogen peroxide is produced in blood plasma and elevation of its level could constitute a pathogenic factor in vascular organ damage attendant upon systemic hypertension.

Abstract-Oxygen free radicals, including hydrogen peroxide, may mediate oxidative stress in target organ tissues and contribute to cardiovascular complications in hypertension. To examine heritability of hydrogen peroxide production, we investigated this trait in a family-based cohort consisting of family members (nϭ236) ascertained through probands (nϭ57) with essential hypertension. Significant effects on hydrogen peroxide production were found for gender and ethnicity, with men having greater values than women (PϽ0.001) and white subjects having greater values than black subjects (Pϭ0.025). Hydrogen peroxide production correlated directly with plasma renin activity (Pϭ0.015), suggesting an important interaction between circulating oxygen radicals and the renin-angiotensin system and a potential mechanism for lower hydrogen peroxide values observed in blacks. Heritability estimates from familial correlations revealed that approximately 20% to 35% of the observed variance in hydrogen peroxide production could be attributed to genetic factors, suggesting a substantial heritable component to the overall determination of this trait. Hydrogen peroxide production negatively correlated with cardiac contractility (rϭϪ0.214, Pϭ0.001) and renal function (rϭϪ0.194, Pϭ0.003). In conclusion, these results indicate that hydrogen peroxide production is heritable and is related to target organ function in essential hypertension. Genetic loci influencing hydrogen peroxide production may represent logical candidates to investigate as susceptibility genes for cardiovascular target organ injury. Key Words: genetics Ⅲ hypertension, essential Ⅲ oxygen free radicals T here is increasing evidence that reactive oxygen species such as superoxide, hydrogen peroxide, and the hydroxyl radical may play a role in the development of organ damage associated with cardiovascular disease in general and hypertension in particular. We recently found evidence to suggest that hypertensive patients exhibit a significantly higher production of plasma peroxide than normotensive subjects. 1 In addition, among still-normotensive subjects, those with a family history of hypertension have a higher production of plasma peroxide than those normotensives without a family history of hypertension. These findings suggest that there may be a genetic component that leads to elevated production of hydrogen peroxide. A number of recent studies in experimental models with genetic forms of hypertension (spontaneously hypertensive rats, saltdependent Dahl hypertensive rats) have also demonstrated a significantly enhanced level of oxidative stress in the endothelial cells of arteriolar as well as venular segments of the circulation. [2][3][4][5] These studies in genetic models of hypertension also suggest the hypothesis that a phenotype associated with an enhanced level of oxidative stress may ultimately have a heritable component in hypertension.We therefore investigated hydrogen peroxide production in a family-based cohort, ascertained through probands with essential ...

Enhanced production of oxygen free radicals may play a role in hypertension by affecting vascular smooth muscle contraction, resistance to blood flow, and organ damage. The aim of this study was to determine whether oxygen free radicals are involved in the development of salt-induced hypertension. Dahl salt-sensitive (Dahl-S) and salt-resistant (Dahl-R) rats were fed either a high salt (6.0% NaCl) or low salt (0.3% NaCl) diet for 4 weeks. The high salt diet caused the development of severe hypertension in Dahl-S animals and had no effect on blood pressure in Dahl-R animals. A tetranitroblue tetrazolium dye was used to detect superoxide radicals in microvessels of the mesentery. Light absorption measurements revealed enhanced staining along the endothelium of arterioles and venules in hypertensive Dahl-S animals, with significantly lower values in normotensive animals. In addition, a Clark electrochemical electrode was used to measure hydrogen peroxide levels in fresh plasma. Hypertensive Dahl-S animals had a higher plasma hydrogen peroxide concentration compared with their normotensive counterparts (2.81+/-0.43 versus 2.10+/-0.41 micromol/L), while no difference was detected between high- and low salt-treated Dahl-R animals (1.70+/-0.35 versus 1.56+/-0.51 micromol/L). The plasma hydrogen peroxide levels of all groups correlated with mean arterial pressure (r=.77). These findings demonstrate an enhanced production of oxygen free radicals in the microvasculature of hypertensive Dahl-S rats.

Experimental evidence has made it clear that the size of an object can have an effect on its properties. The electrical resistivity of a thin film will become larger as the thickness of that film decreases in size. Furthermore, the electrical resistivity will also increase as the temperature increases. To help understand these relationships, a model is presented, and equations are obtained to help understand the mechanisms responsible for these properties and to give insight into the underlying physics between these parameters. Comparisons are made between experimental data and values generated from the theoretical equations derived from the model. All of this analysis provides validation for the theoretical model. Therefore, since the model is accurate, it provides insight into the underlying physics that relates electrical resistivity to temperature and film thickness.PACS73.61.At; 73.50.Bk; 72.15.Eb; 72.10.d; 63.20.kd.

These findings indicate that xanthine oxidase-derived oxygen free radicals are involved in the pathogenesis of salt-induced hypertension.