scholarly journals Tetrahydrobiopterin improves endothelial dysfunction and vascular oxidative stress in microvessels of intrauterine undernourished rats

2004 ◽  
Vol 558 (1) ◽  
pp. 239-248 ◽  
Author(s):  
Maria do Carmo P. Franco ◽  
Zuleica B. Fortes ◽  
Eliana H. Akamine ◽  
Elisa M. Kawamoto ◽  
Cristoforo Scavone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Vascular Oxidative Stress

Oxidative stress and endothelial dysfunction

2007 ◽  
Vol 27 (01) ◽  
pp. 5-12 ◽  
Author(s):  
G. Muller ◽  
C. Goettsch ◽  
H. Morawietz
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Vascular Function ◽  
Vessel Wall ◽  
Clinical Implications ◽  
Oxygen Species ◽  
Vascular Oxidative Stress ◽  
Arteries And Veins ◽  
Different Sources

SummaryThis review focuses on the role of vascular oxidative stress in the development and progression of endothelial dysfunction. We discuss different sources of oxidative stress in the vessel wall, oxidative stress and coagulation, the role of oxidative stress and vascular function in arteries and veins, the flow-dependent regulation of reactive oxygen species, the putative impact of oxidative stress on atherosclerosis, the interaction of angiotensin II, oxidative stress and endothelial dysfunction, and clinical implications.

scholarly journals Differential contribution of Nox1, Nox2 and Nox4 to kidney vascular oxidative stress and endothelial dysfunction in obesity

Redox Biology ◽  
2020 ◽  
Vol 28 ◽  
pp. 101330 ◽  
Author(s):  
Mercedes Muñoz ◽  
Maria Elvira López-Oliva ◽  
Claudia Rodríguez ◽  
María Pilar Martínez ◽  
Javier Sáenz-Medina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Vascular Oxidative Stress ◽  
Differential Contribution

scholarly journals Contribution of monoamine oxidases to vascular oxidative stress in patients with end-stage renal disease requiring hemodialysis

2017 ◽  
Vol 95 (11) ◽  
pp. 1383-1388 ◽  
Author(s):  
Diana Uțu ◽  
Stelian Pantea ◽  
Oana M. Duicu ◽  
Danina M. Muntean ◽  
Adrian Sturza
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Renal Disease ◽  
Vascular Access ◽  
End Stage Renal Disease ◽  
Mao Inhibitors ◽  
Monoamine Oxidases ◽  
Stage Renal Disease ◽  
End Stage ◽  
Vascular Oxidative Stress

Arteriovenous fistula (AVF) is the “lifeline” for patients with end-stage renal disease (ESRD) undergoing hemodialysis. AVF maturation failure is a poorly understood process, one of the contributors being endothelial dysfunction due to oxidative stress. Monoamine oxidases (MAOs) A and B were recently identified as novel sources of vascular oxidative stress. The aim of the present study was to assess the contribution of MAOs to the endothelial dysfunction in patients with ESDR with indication of hemodialysis. Fragments of brachial artery collaterals were harvested from ESRD patients during the surgical procedure aimed at creating the vascular access in the cubital fossa. The effect of increasing concentrations (10, 30, 100 μmol/L) of the irreversible MAO-A inhibitor, clorgyline, and MAO-B inhibitor, selegiline, on endothelial-dependent relaxation (EDR) in response to cumulative doses of acetylcholine was studied in isolated phenylephrine-preconstricted vascular rings. Hydrogen peroxide (H2O2) production was assessed using ferrous oxidation xylenol orange assay. We showed that incubation of brachial rings with MAO inhibitors significantly improved EDR and attenuated H2O2 generation in patients with ESRD. MAO-related oxidative stress might contribute to the primary dysfunction/non-maturation of the AVF and MAO inhibitors could improve maturation and long-term patency of the vascular access in dialysis patients.

scholarly journals Vascular Oxidative Stress and Endothelial Dysfunction in Patients With Chronic Heart Failure

Circulation ◽  
2002 ◽  
Vol 106 (24) ◽  
pp. 3073-3078 ◽  
Author(s):  
Ulf Landmesser ◽  
Stephan Spiekermann ◽  
Sergey Dikalov ◽  
Helma Tatge ◽  
Ragna Wilke ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Endothelial Dysfunction ◽  
Vascular Oxidative Stress

Abstract P182: Advanced Atherosclerosis is Associated with Systemic and End-organ Inflammation, Vascular Oxidative Stress and Endothelial Dysfunction but not Hypertension in Mice

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Quynh N Dinh ◽  
Grant R Drummond ◽  
Henry Diep ◽  
Christopher T Chan ◽  
Dorota Ferens ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
High Fat ◽  
Chronic Inflammatory Condition ◽  
Tnf Α ◽  
Brain Expression ◽  
Cytokine Levels ◽  
Ifn Γ ◽  
Vascular Oxidative Stress

Introduction: Evidence suggests that hypertension involves underlying inflammation, however whether atherosclerosis - a chronic inflammatory condition - can cause hypertension is unknown. We tested whether blood pressure (BP) is higher in high-fat fed ApoE-/- vs chow-fed wild-type (WT) mice, and whether advanced atherosclerosis is associated with systemic and end-organ inflammation, oxidative stress and endothelial dysfunction. Methods: Male ApoE-/- and WT mice were placed on high fat and chow diets, respectively, from 5-56 weeks. To clarify the effects of ageing alone, aged WT mice were compared to young chow-fed WT mice (8-12 week old). We measured systolic BP, plasma cytokine levels, mRNA expression of inflammatory markers, vascular superoxide and endothelial function. Results: There was no difference in BP of aged ApoE-/- (104.2 ± 2.9 mmHg) and age-matched WT mice (113.2 ± 1.3 mmHg) (n=13-18, P>0.05). However, plasma IL-6, TNF-α and IFN-γ were elevated in ApoE-/- by more than 2-fold vs age-matched WT (n=9-10, all P<0.05), as was brain expression of IL-1β, IL-6, TNF-α, IFN-γ, TGFβ1, CCR2, CCL2, CCL7, CCL8, CCL12 and IL-10 (n=9-10, all P<0.05), and aortic expression of IL-6, CCR2, CCL8 and CCL12 (n=6-8, all P<0.05). Ageing, but not atherosclerosis, increased renal expression of IL-1β, IL-6, TNF-α, CCR2, CCL2, CCL7, CCL8, CCL12 and Foxp3, and aortic expression of CCL2, IL-10 and Foxp3 by at least 2-fold (n=6-10, all P<0.05). In ApoE-/- aorta, Nox2-dependent superoxide production was 4-fold greater than in WT (n=5-6, P<0.05), and endothelium-dependent vasorelaxation to carbachol was markedly reduced by more than half (n=5-7, P<0.05). Ageing alone had no effect on BP, systemic inflammation or endothelial function. Conclusions: Despite the systemic and end-organ inflammation, oxidative stress and endothelial dysfunction, advanced atherosclerosis does not result in elevated BP.

scholarly journals Nanoparticles in Medicine: A Focus on Vascular Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-20 ◽  
Author(s):  
M. D. Mauricio ◽  
S. Guerra-Ojeda ◽  
P. Marchio ◽  
S. L. Valles ◽  
M. Aldasoro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Biomedical Applications ◽  
Vascular Tone ◽  
Vascular Dysfunction ◽  
Antioxidant Properties ◽  
Cell Toxicity ◽  
No Bioavailability ◽  
Vascular Alteration ◽  
Vascular Oxidative Stress

Nanotechnology has had a significant impact on medicine in recent years, its application being referred to as nanomedicine. Nanoparticles have certain properties with biomedical applications; however, in some situations, they have demonstrated cell toxicity, which has caused concern surrounding their clinical use. In this review, we focus on two aspects: first, we summarize the types of nanoparticles according to their chemical composition and the general characteristics of their use in medicine, and second, we review the applications of nanoparticles in vascular alteration, especially in endothelial dysfunction related to oxidative stress. This condition can lead to a reduction in nitric oxide (NO) bioavailability, consequently affecting vascular tone regulation and endothelial dysfunction, which is the first phase in the development of cardiovascular diseases. Therefore, nanoparticles with antioxidant properties may improve vascular dysfunction associated with hypertension, diabetes mellitus, or atherosclerosis.

scholarly journals Endothelial SHIP2 Suppresses Nox2 NADPH Oxidase–Dependent Vascular Oxidative Stress, Endothelial Dysfunction, and Systemic Insulin Resistance

Diabetes ◽  
2017 ◽  
Vol 66 (11) ◽  
pp. 2808-2821 ◽  
Author(s):  
Nicole T. Watt ◽  
Matthew C. Gage ◽  
Peysh A. Patel ◽  
Hema Viswambharan ◽  
Piruthivi Sukumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Systemic Insulin Resistance ◽  
Vascular Oxidative Stress

scholarly journals Heme Oxygenase-1 Induction and Organic Nitrate Therapy: Beneficial Effects on Endothelial Dysfunction, Nitrate Tolerance, and Vascular Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Andreas Daiber ◽  
Matthias Oelze ◽  
Philip Wenzel ◽  
Franziska Bollmann ◽  
Andrea Pautz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Endothelial Dysfunction ◽  
Heme Oxygenase ◽  
Nitrate Tolerance ◽  
Heme Oxygenase 1 ◽  
Organic Nitrate ◽  
Organic Nitrates ◽  
Beneficial Effects ◽  
Vascular Oxidative Stress

Organic nitrates are a group of very effective anti-ischemic drugs. They are used for the treatment of patients with stable angina, acute myocardial infarction, and chronic congestive heart failure. A major therapeutic limitation inherent to organic nitrates is the development of tolerance, which occurs during chronic treatment with these agents, and this phenomenon is largely based on induction of oxidative stress with subsequent endothelial dysfunction. We therefore speculated that induction of heme oxygenase-1 (HO-1) could be an efficient strategy to overcome nitrate tolerance and the associated side effects. Indeed, we found that hemin cotreatment prevented the development of nitrate tolerance and vascular oxidative stress in response to chronic nitroglycerin therapy. Vice versa, pentaerithrityl tetranitrate (PETN), a nitrate that was previously reported to be devoid of adverse side effects, displayed tolerance and oxidative stress when the HO-1 pathway was blocked pharmacologically or genetically by using HO-1+/–mice. Recently, we identified activation of Nrf2 and HuR as a principle mechanism of HO-1 induction by PETN. With the present paper, we present and discuss our recent and previous findings on the role of HO-1 for the prevention of nitroglycerin-induced nitrate tolerance and for the beneficial effects of PETN therapy.

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