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. 2023 Jan 10;13:1098725. doi: 10.3389/fimmu.2022.1098725

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Copyright © 2023 Zhang, Zhao, Zhou, Meng and Zhou

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanisms of oxidative stress causing hypertension in vascular endothelial cells. Ang II and ET-1 can stimulate NADPH oxidase and mitochondria to produce ROS (e.g., H2O2 and OFR), which are recognized by their receptors on the endothelial cells. ROS stimulate the PI3K/Akt-MAPK pathway to inhibit the expression of eNOS mRNA and eNOS activity, thus reducing the availability of NO, which results in vasodilation insufficiency and elevation of blood pressure. Moreover, angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs) and vitamin C (VC) may be potential therapeutic strategies in the process of oxidative stress.