Oxidative stress and vascular damage in hypertension

Berry, Colin; Brosnan, M J; Fennell, Jérôme; Hamilton, Carlene A.; Dominiczak, Anna F.

doi:10.1097/00041552-200103000-00014

Cited by 130 publications

(85 citation statements)

References 83 publications

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“…27 There is also some evidence for similar mechanisms in human endothelial dysfunction and essential hypertension. 28,29 Although an alternative explanation may be that changes in the levels of Gstm2 expression between the strains are secondary to blood pressure differences already present in 15-week-old rats.…”

Section: Discussionmentioning

confidence: 99%

Microarray Analysis of Rat Chromosome 2 Congenic Strains

et al. 2003

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Abstract-Human essential hypertension is a complex polygenic trait with underlying genetic components that remain unknown. The stroke-prone spontaneously hypertensive rat (SHRSP) is a model of human essential hypertension, and a number of reproducible blood pressure regulation quantitative trait loci have been found to map to rat chromosome 2. The SP.WKYGla2c* congenic strain was produced by introgressing a region of rat chromosome 2 from the normotensive Wistar Kyoto (WKY) strain into the genetic background of the SHRSP.

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Section: Discussionmentioning

confidence: 99%

Microarray Analysis of Rat Chromosome 2 Congenic Strains

et al. 2003

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“…NO plays a key role in the maintenance of vascular tone and BP. 42,43 Some studies have shown that FFAs can impair eNOS activity and EDV in vitro. In humans, EDV and NO production were impaired when plasma NEFAs were increased with Intralipid+heparin.…”

Section: Discussionmentioning

confidence: 99%

Role of oxidative stress in elevated blood pressure induced by high free fatty acids

Wang

Hou

et al. 2009

Hypertens Res

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The aim of the study is to investigate the possible mechanism of oxidative stress in the high free fatty acids (FFAs)-induced hypertension. Male Sprague-Dawley rat models were established and classified into three groups, namely the control group (NC group), the FFA group, and the N-acetylcysteine (NAC) group. Blood pressure (BP) was recorded. An organ chamber experiment was performed to determine endothelium-dependent/-independent vasodilation (EDV/EIV). Reactive oxygen species (ROS), nitrotyrosine, reduced glutathione hormone (GSH) and NO 2 À /NO 3 À levels were measured in plasma. Endothelial nitric oxide synthase (eNOS) mRNA expression in endothelial cells was evaluated by real-time PCR. The following results were observed: (1) In the FFA group, BP increased after 4 h infusion of Intralipid+heparin. In the NAC group, systolic and diastolic BP remained the same. (2) In the FFA group, the aortic rings tended to show impaired EDV in response to acetylcholine (ACh). There was no difference of EDV response in the NAC and NC groups. (3) In the FFA group, NO 2 À /NO 3 À levels were significantly reduced, and eNOS mRNA expression and activity were significantly decreased compared with the NC group. NAC administration increased eNOS mRNA expression and activity. (4) ROS and nitrotyrosine concentrations in the FFA group were higher than in the NC group, and GSH concentrations in the FFA group were lower than in the NC group. Elevated FFAs can induce elevated BP, potentially through FFA-induced impairment of EDV resulting from decreased eNOS mRNA expression and activity. Oxidative stress may also play an important role in potential mechanisms of this high FFA-induced elevated BP.

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“…␣-Tocopherol improved endothelial function in patients with type I diabetes mellitus, those with spastic angina, hypercholesterolemic patients who smoke cigarettes, and hyperhomocysteinemic subjects. 43,44 Vitamin C administration also improves endothelium-dependent vasodilation in patients with hypertension, hypercholesterolemia, diabetes mellitus, coronary artery disease, and hyperhomocysteinemia (see reviews 43,44 ). In the same line of evidence, it has been postulated that smokers have lower levels of plasma vitamin C than do nonsmokers; this difference has been associated with endothelial dysfunction.…”

Section: Pharmacological Perspectivesmentioning

confidence: 99%

Heart Failure, Redox Alterations, and Endothelial Dysfunction

2001

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Abstract-Heart failure is characterized by neurohumoral alterations, such as activation of the sympathetic nervous system, stimulation of the renin-angiotensin system, increased activity of the endothelin system, increased production of norepinephrine, and increased circulating levels of cytokines. Oxidative stress is associated with the formation of reactive oxygen species (ROS). The myocardium has enzymes that stimulate ROS generation and enzymes with antioxidant effects. Several studies have suggested that ROS are increased in the failing heart. ROS may contribute to the pathophysiology of heart failure by initiating myocyte apoptosis and exerting direct negatively inotropic effects through the reduction of cytosolic intracellular free calcium. However, mechanisms such as endothelial dysfunction and inflammation have also been involved in the progression of heart failure. Antioxidants (eg, vitamin C) seem to improve endothelial functionality and reduce the inflammatory response in patients with heart failure. Therefore, in this review, we analyzed the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure.

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Oxidative stress and vascular damage in hypertension

Cited by 130 publications

References 83 publications

Microarray Analysis of Rat Chromosome 2 Congenic Strains

Microarray Analysis of Rat Chromosome 2 Congenic Strains

Role of oxidative stress in elevated blood pressure induced by high free fatty acids

Heart Failure, Redox Alterations, and Endothelial Dysfunction

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