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Curr Hypertens Rev. 2019 May 30. doi: 10.2174/1573402115666190531071924. [Epub ahead of print]

Sources and effects of oxidative stress in hypertension.

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Department of Psychiatric Nursing and Human Sciences, Ribeirao Preto College of Nursing, University of Sao Paulo. Brazil.
Wilf Family Cardiovascular Research Institute, Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, New York. United States.



Disbalance of reactive oxygen species production (ROS) are central in several diseases. In hypertension, is well known the increase in ROS production, mainly by NADPH oxidases and xanthine oxidoreductase, among others, activated by a myriad of mechanisms. Concomitantly, occurs decrease of antioxidant defenses, enzymatic and non-enzymatic. The participation of ROS in development of hypertension is clear, although still unclear if ROS are cause or consequence in tissue changes in hypertension. Disbalance of ROS cause several changes in tissue, since removing nitric oxide (NO) produced from endothelial, activation of metalloproteinases, until direct tissue damage by reaction with lipids, proteins and DNA. Thus, to understand hypertension are critical know the participation of ROS in this disease.


This minireview discuss the mainly enzymatic sources of oxidants and the major antioxidant defenses in vasculature followed by the molecular effects of disbalance of ROS in hypertension, highlighting endothelial dysfunction, vascular remodeling and tissue damage.


Hypertension; MMP; Oxidative stress; endothelial dysfunction

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