The role of oxidative stress in the pathophysiology of hypertension
Open accessAbstract
Hypertension is considered to be the most important risk factor in the development of cardiovascular disease. An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. The bioavailability of nitric oxide (NO), which is a major vasodilator, is highly dependent on the redox status. Under physiological conditions, low concentrations of intracellular ROS have an important role in the normal redox signaling maintaining vascular function and integrity. However, under pathophysiological conditions, increased levels of ROS contribute to vascular dysfunction and remodeling through oxidative damage. In human hypertension, an increase in the production of superoxide anions and hydrogen peroxide, a decrease in NO synthesis and a reduction in antioxidant bioavailability have been observed. In turn, antioxidants are reducing agents that can neutralize these oxidative and otherwise damaging biomolecules. The use of antioxidant vitamins, such as vitamins C and E, has gained considerable interest as protecting agents against vascular endothelial damage. Available data support the role of these vitamins as effective antioxidants that can counteract ROS effects. This review discusses the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of vascular damage in hypertension, and the possible therapeutic strategies that could prevent or treat this disorder.
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Oxidative stress may play a role in the development of vascular complications that promote cardiovascular disease by contributing to the pathogenesis of hypertension and atherosclerosis.
“Oxidative stress may play a role in the development of vascular complications that promote cardiovascular disease by contributing to the pathogenesis of hypertension [143,144] and atherosclerosis [145].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [144]
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- Authors
- Rodrigo, R., González, J., & Paoletto, F.
- Affiliations
- University of Chile (CL)
- Corresponding author
- Rodrigo, Ramón
- ORCID
- Rodrigo, Ramón
- Venue
- Hypertension Research
- Published
- 2011-01-13
- Volume
- 34
- Issue
- 4
- Pages
- 431-440
- ISSN
- 0916-9636 (ISSN-L)
- 1348-4214
- OpenAlex
- W2065634680
- Cited by
- 436
- References
- 164
- Citations by year
- 2026: 6 · 2025: 33 · 2024: 35 · 2023: 60 · 2022: 52 · 2021: 47 · 2020: 44 · 2019: 26 · 2018: 19 · 2017: 18 · 2016: 15 · 2015: 21 · 2014: 19 · 2013: 17 · 2012: 21
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Hypertension Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- oxidative stress, hypertension, reactive oxygen species, nitric oxide bioavailability, vascular dysfunction, vascular remodeling, antioxidant vitamins, vitamin C, vitamin E, angiotensin II, endothelin-1, urotensin II, superoxide, hydrogen peroxide, antioxidant therapy
- MeSH terms
- Antioxidants, Blood Pressure, Cardiovascular System, Humans, Hypertension, Reactive Oxygen Species, Oxidative Stress
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