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Review
. 2017 Jan;101(1):169-193.
doi: 10.1016/j.mcna.2016.08.004. Epub 2016 Oct 27.

Oxidative Stress and Hypertensive Diseases

Roxana Loperena  1 , David G Harrison  2
Affiliations
Review

Oxidative Stress and Hypertensive Diseases

Roxana Loperena et al. Med Clin North Am. 2017 Jan.

Abstract

It has become clear that reactive oxygen species (ROS) contribute to the development of hypertension via myriad effects. ROS are essential for normal cell function; however, they mediate pathologic changes in the brain, the kidney, and blood vessels that contribute to the genesis of chronic hypertension. There is also emerging evidence that ROS contribute to immune activation in hypertension. This article discusses these events and how they coordinate to contribute to hypertension and its consequent end-organ damage.

Keywords: Dendritic cells; Hydrogen peroxide; NADPH oxidase; Renal; Superoxide; Sympathetic nerves; Vascular.

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Figures

Figure 1
Figure 1
Sources and formation of reactive oxygen species in mammalian cells that are relevant to hypertension.
Figure 2
Figure 2
Renal effects of ROS and NO.
Figure 3
Figure 3
Sites in the brain implicated in hypertension. Shown also are documented actions of ROS and NO to modulate central control of blood pressure.
Figure 4
Figure 4
Mechanisms by which ROS and NO modulate vascular function and structure in hypertension.
Figure 5
Figure 5
Formation of isolevuloglandins in antigen presenting cells and modification of self-proteins leading to T cell activation.
Figure 6
Figure 6
Interplay between immune activation, the central nervous system, the vasculature and the kidney in hypertension.
See this image and copyright information in PMC

References

    1. Liochev SI. Reactive oxygen species and the free radical theory of aging. Free Radic Biol Med. 2013;60:1–4. - PubMed
    1. Shin MH, Moon YJ, Seo JE, Lee Y, Kim KH, Chung JH. Reactive oxygen species produced by NADPH oxidase, xanthine oxidase, and mitochondrial electron transport system mediate heat shock-induced MMP-1 and MMP-9 expression. Free Radic Biol Med. 2008;44:635–645. - PubMed
    1. Semchyshyn HM. Reactive carbonyl species in vivo: generation and dual biological effects. ScientificWorldJournal. 2014;2014:417842. - PMC - PubMed
    1. Kirabo A, Fontana V, de Faria AP, Loperena R, Galindo CL, Wu J, Bikineyeva AT, Dikalov S, Xiao L, Chen W, Saleh MA, Trott DW, Itani HA, Vinh A, Amarnath V, Amarnath K, Guzik TJ, Bernstein KE, Shen XZ, Shyr Y, Chen SC, Mernaugh RL, Laffer CL, Elijovich F, Davies SS, Moreno H, Madhur MS, Roberts J, 2nd, Harrison DG. DC isoketal-modified proteins activate T cells and promote hypertension. J Clin Invest. 2014;124:4642–4656. - PMC - PubMed
    1. Guzik TJ, Chen W, Gongora MC, Guzik B, Lob HE, Mangalat D, Hoch N, Dikalov S, Rudzinski P, Kapelak B, Sadowski J, Harrison DG. Calcium-dependent NOX5 nicotinamide adenine dinucleotide phosphate oxidase contributes to vascular oxidative stress in human coronary artery disease. J Am Coll Cardiol. 2008;52:1803–1809. - PMC - PubMed

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