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Hypertension: Mechanisms of Oxidative Stress and Antioxidant Regulation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 October 2024) | Viewed by 1088

Special Issue Editor


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Guest Editor
Department of Translational Research on New Technologies in Medicine and Surgery, University of Pisa, Via S. Zeno 31, 56127 Pisa, Italy
Interests: blood pressure; hypertension; antioxidants

Special Issue Information

Dear Colleagues,

Arterial hypertension is known as one of the main chronic diseases, affecting more than 1 billion people worldwide. The complications of this disease include cerebro-vascular stroke, coronary artery disease, heart failure, and kidney disease. These are major causes of morbidity and mortality all around the world. However, arterial blood pressure reduction in hypertensive people can prevent or drastically reduce these complications. Recent studies that were carried out on both humans and animal models showed that the increase in blood pressure is, at least in part, caused by an alteration of the endothelium at the level of the arterioles. This alteration is mainly due to an imbalance between the oxidizing and antioxidant substances normally produced by the body. An increase in oxidant substances, particularly reactive oxygen species (ROS), induces deterrent effects by triggering a cascade of signals that result in endothelial dysfunction that promotes the progression of cardiovascular disorders. Another important aspect is that the increase in pressure determines a geometric rearrangement of the vascular networks, impairing tissue perfusion.

The main aim of this Special Issue is to provide a broad overview of the mechanisms through which oxidative stress causes cardiovascular disorders and analyze the mechanisms underlying the regulatory effects of antioxidative natural substances. We warmly welcome submissions, including original papers and reviews, on this topic of such important public health interest.

Dr. Rossana Scuri
Guest Editor

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Keywords

  • arteriolar networks organization
  • blood flow supply
  • cardiovascular disease
  • endothelial dysfunction
  • eNOS regulatory activity
  • oxidative stress
  • polyphenols

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Published Papers (2 papers)

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Research

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13 pages, 3150 KiB  
Article
L-Arginine and Taurisolo® Effects on Brain Hypoperfusion–Reperfusion Damage in Hypertensive Rats
by Dominga Lapi, Gian Carlo Tenore, Giuseppe Federighi, Martina Chiurazzi, Santo Nunziato, Maria S. Lonardo, Mariano Stornaiuolo, Antonio Colantuoni, Ettore Novellino and Rossana Scuri
Int. J. Mol. Sci. 2024, 25(19), 10868; https://doi.org/10.3390/ijms251910868 - 9 Oct 2024
Viewed by 758
Abstract
Acute and chronic hypertension causes cerebral vasculopathy, increasing the risk of ischemia and stroke. Our study aimed to compare the effects of arterial pressure reduction on the pial microvascular responses induced by hypoperfusion and reperfusion in spontaneously hypertensive Wistar rats, desamethasone-induced hypertensive Wistar [...] Read more.
Acute and chronic hypertension causes cerebral vasculopathy, increasing the risk of ischemia and stroke. Our study aimed to compare the effects of arterial pressure reduction on the pial microvascular responses induced by hypoperfusion and reperfusion in spontaneously hypertensive Wistar rats, desamethasone-induced hypertensive Wistar rats and age-matched normotensive Wistar rats fed for 3 months with a normal diet or normal diet supplemented with L-arginine or Taurisolo® or L-arginine plus Taurisolo®. At the end of treatments, the rats were submitted to bilateral occlusion of common carotid arteries for 30 min and reperfusion. The microvascular parameters investigated in vivo through a cranial window were: arteriolar diameter changes, permeability increase, leukocyte adhesion to venular walls and percentage of capillaries perfused. Hypoperfusion–reperfusion caused in all rats marked microvascular changes. L-arginine treatment was effective in reducing arterial blood pressure causing vasodilation but did not significantly reduce the damage induced by hypoperfusion–reperfusion. Taurisolo® treatment was less effective in reducing blood pressure but prevented microvascular damage from hypoperfusion–reperfusion. L-arginine plus Taurisolo® maintained blood pressure levels within the physiological range and protected the pial microcirculation from hypoperfusion–reperfusion-induced microvascular injuries. Therefore, the blood pressure reduction is not the only fundamental aspect to protect the cerebral circulation from hypoperfusion–reperfusion damage. Full article
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Review

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16 pages, 1831 KiB  
Review
Oxidative DNA Damage and Arterial Hypertension in Light of Current ESC Guidelines
by Radka Hazuková, Zdeněk Zadák, Miloslav Pleskot, Petr Zdráhal, Martin Pumprla and Miloš Táborský
Int. J. Mol. Sci. 2024, 25(23), 12557; https://doi.org/10.3390/ijms252312557 - 22 Nov 2024
Abstract
A new insight into oxidative stress is based on oxidative deoxyribonucleic acid (DNA) damage. DNA is the pivotal biopolymer for life and health. Arterial hypertension (HT) is a globally common disease and a major risk factor for numerous cardiovascular (CV) conditions and non-cardiac [...] Read more.
A new insight into oxidative stress is based on oxidative deoxyribonucleic acid (DNA) damage. DNA is the pivotal biopolymer for life and health. Arterial hypertension (HT) is a globally common disease and a major risk factor for numerous cardiovascular (CV) conditions and non-cardiac complications, making it a significant health and socio-economic problem. The aetiology of HT is multifactorial. Oxidative stress is the main driver. Oxidative DNA damage (oxidised guanosine (8OHdG), strand breaks (SSBs, DSBs)) seems to be the crucial and initiating causal molecular mechanism leading to HT, acting through oxidative stress and the resulting consequences (inflammation, fibrosis, vascular remodelling, stiffness, thickness, and endothelial dysfunction). In light of the current European Society of Cardiology (ESC) guidelines with defined gaps in the evidence, this manuscript, for the first time, (1) summarizes evidence for oxidative DNA damage in HT and other CV risk factors, (2) incorporates them into the context of known mechanisms in HT genesis, (3) proposes the existing concept of HT genesis innovatively supplemented with oxidative DNA damage, and (4) mentions consequences such as promising new targets for the treatment of HT (DNA damage response (DDR) pathways). Full article
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