scholarly journals Oxidative Stress in Hypertensive Patients Induces an Increased Contractility in Vein Grafts Independent of Endothelial Function

2011 ◽  
Vol 2011 ◽  
pp. 1-8
Author(s):  
Claudio Joo Turoni ◽  
Rodrigo Marañón ◽  
Maria Karbiner ◽  
Juan Muntaner ◽  
Víctor Proto ◽  
...  

Objective. To evaluate the impact of oxidative stress on vascular reactivity to vasoconstrictors and on nitric oxide (NO) bioavailability in saphenous vein (SV) graft with endothelial dysfunction from hypertensive patients (HT).Methods. Endothelial function, vascular reactivity, oxidative state, nitrites and NO release were studied in isolated SV rings from HT and normotensive patients (NT). Only rings with endothelial dysfunction were used.Results. HT rings presented a hyperreactivity to vasoconstrictors that was reverted by diphenylene iodonium (DPI). In NT, no effect of DPI was obtained, but Nω-nitro-L-arginine methyl ester (L-NAME) increased the contractile response. NO was present in SV rings without endothelial function. Nitrites were higher in NT than in HT (1066.1 ± 86.3 pmol/mg;n=11versus 487.8 ± 51.6;n=23;P<0.01) and inhibited by nNOS inhibitor. L-arginine reversed this effect. Antioxidant agents increased nitrites and NO contents only in HT. The anti-nNOS-stained area by immunohistochemistry was higher in NT than HT. HT showed an elevation of oxidative state.Conclusions. Extraendothelial NO counter-regulates contractility in SV. However, this action could be altered in hypertensive situations by an increased oxidative stress or a decreased ability of nNOS to produce NO. Further studies should be performed to evaluate the implication of these results in graft patency rates.

2021 ◽  
Author(s):  
Patrizia Dardi ◽  
Laís Rossi Perazza ◽  
Gisele Kruger Couto ◽  
Gianne Paul Campos ◽  
Luciano dos Santos Aggum Capettini ◽  
...  

Arterial endothelial dysfunction has been extensively studied in heart failure (HF). However little is known about the adjustments shown by the venous system in this condition. Considering that inferior vena cava (VC) tone could influence cardiac performance and HF prognosis, the aim of the present study was to assess the VC and thoracic aorta (TA) endothelial function of HF-post-myocardial infarction (MI) rats, comparing both endothelial responses and signaling pathways developed. Vascular reactivity of TA and VC from HF post-MI and sham operated (SO) rats was assessed with a wire myograph, four weeks after coronary artery occlusion surgery. Nitric oxide (NO), H2O2 production and oxidative stress were evaluated in situ with fluorescent probes, whilst protein expression and dimer/monomer ratio was assessed by western blot. VC from HF rats presented endothelial dysfunction, while TA exhibited higher acetylcholine (ACh)-induced vasodilation when compared to vessels from SO rats. TA exhibited increased ACh-induced NO production due to a higher coupling of endothelial and neuronal NO synthases isoforms (eNOS, nNOS), and enhanced expression of antioxidant enzymes. These adjustments, however, were absent in VC of HF post-MI rats, which exhibited uncoupled nNOS, oxidative stress and higher H2O2 bioavailability. Altogether, this study suggests a differential regulation of endothelial function between VC and TA of HF post-MI rats, most likely due to nNOS uncoupling and compromised antioxidant defense.


2012 ◽  
Vol 25 (2) ◽  
pp. 288-301 ◽  
Author(s):  
Sébastien Lacroix ◽  
Christine Des Rosiers ◽  
Jean-Claude Tardif ◽  
Anil Nigam

Endothelial dysfunction is a turning point in the initiation and development of atherosclerosis and its complications and is predictive of future cardiovascular events. Ingestion of high-carbohydrate or high-fat meals often results in postprandial hyperglycaemia and/or hypertriacylglycerolaemia that may lead to a transient impairment in endothelial function. The present review will discuss human studies evaluating the impact of high-carbohydrate and high-fat challenges on postprandial endothelial function as well as the potential role of oxidative stress in such postprandial metabolic alterations. Moreover, the present review will differentiate the postprandial endothelial and oxidative impact of meals rich in varying fatty acid types.


2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.


2021 ◽  
Vol 27 (2) ◽  
pp. 133-145
Author(s):  
E. N. Dudinskaya ◽  
L. V. Matchekhina ◽  
K. A. Eruslanova ◽  
O. A. Dogotar ◽  
L. P. Ryltseva ◽  
...  

The review summarizes the data of past two decades on the effect of hypertension on vascular aging and considers the effect of chronic inflammation and oxidative stress patterns on the remodeling of cardiovascular system. Clinical studies on the effect of various classes of antihypertensive drugs on age-associated parameters of vascular aging are discussed. These include endothelial dysfunction and arterial assessed by endothelium-dependent vasodilation, pulse wave velocity, augmentation index, cardiovascular index, thickness of the intima-media complex, and so on.


2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Sebastian Steven ◽  
Matthias Oelze ◽  
Moritz Brandt ◽  
Elisabeth Ullmann ◽  
Swenja Kröller-Schön ◽  
...  

Objective. Oxidative stress and endothelial dysfunction contribute to pulmonary arterial hypertension (PAH). The role of the nitrovasodilator pentaerythritol tetranitrate (PETN) on endothelial function and oxidative stress in PAH has not yet been defined.Methods and Results. PAH was induced by monocrotaline (MCT, i.v.) in Wistar rats. Low (30 mg/kg; MCT30), middle (40 mg/kg; MCT40), or high (60 mg/kg; MCT60) dose of MCT for 14, 28, and 42 d was used. MCT induced endothelial dysfunction, pulmonary vascular wall thickening, and fibrosis, as well as protein tyrosine nitration. Pulmonary arterial pressure and heart/body and lung/body weight ratio were increased in MCT40 rats (28 d) and reduced by oral PETN (10 mg/kg, 24 d) therapy. Oxidative stress in the vascular wall, in the heart, and in whole blood as well as vascular endothelin-1 signaling was increased in MCT40-treated rats and normalized by PETN therapy, likely by upregulation of heme oxygenase-1 (HO-1). PETN therapy improved endothelium-dependent relaxation in pulmonary arteries and inhibited endothelin-1-induced oxidative burst in whole blood and the expression of adhesion molecule (ICAM-1) in endothelial cells.Conclusion. MCT-induced PAH impairs endothelial function (aorta and pulmonary arteries) and increases oxidative stress whereas PETN markedly attenuates these adverse effects. Thus, PETN therapy improves pulmonary hypertension beyond its known cardiac preload reducing ability.


2005 ◽  
Vol 18 (5) ◽  
pp. A178-A178
Author(s):  
S COTTONE ◽  
M GUARNERI ◽  
R ARSENA ◽  
A PALERMO ◽  
A VADALA ◽  
...  

2010 ◽  
Vol 298 (5) ◽  
pp. H1600-H1607 ◽  
Author(s):  
Jordan D. Miller ◽  
Veronica A. Peotta ◽  
Yi Chu ◽  
Robert M. Weiss ◽  
Kathy Zimmerman ◽  
...  

Endothelial function is impaired by oxidative stress in chronic heart failure (HF). Mechanisms that protect against increases in oxidative stress in HF are not clear. The goal of this study was to determine whether manganese superoxide dismutase (MnSOD) plays a key role in protecting against endothelial dysfunction in HF. Endothelial function and gene expression were examined in aorta from wild-type mice (MnSOD+/+) and mice deficient in MnSOD (MnSOD+/−) 12 wk after ligation of the left coronary artery (LCA). LCA ligation produced similar size myocardial infarctions in MnSOD+/+ and MnSOD+/− mice and reduced ejection fraction to ∼20% in both groups. Maximal relaxation in response to acetylcholine was 78 ± 3% (mean ± SE) and 66 ± 8% in sham-operated MnSOD+/+ and MnSOD+/− mice, respectively. Expression of antioxidant enzymes increased in MnSOD+/+ mice with HF, and maximal relaxation to acetylcholine was slightly impaired (68 ± 4%). Greater endothelial dysfunction was observed in MnSOD+/− mice with HF (46 ± 5%, P < 0.05), which was significantly improved by polyethylene glycol-catalase but not Tempol. Incubation with the nonspecific cyclooxygenase (COX) inhibitor indomethacin or the COX1 inhibitor valeryl salicylate, but not the COX-2 inhibitor NS-398, significantly improved relaxation to acetylcholine in HF mice (maximum relaxation = 74 ± 5, 91 ± 1, and 58 ± 5%). These data suggest that MnSOD plays a key role in protecting against endothelial dysfunction in HF. A novel mechanism was identified whereby chronic increases in oxidative stress, produced by mitochondrial SOD deficiency, impair vascular function via a hydrogen peroxide-dependent, COX1-dependent, endothelium-derived contracting factor.


2017 ◽  
Vol 95 (8) ◽  
pp. 705-712
Author(s):  
Olga L. Belaya ◽  
K. Yu. Bondar ◽  
L. I. Markova ◽  
Z. V. Kuropteva ◽  
L. M. Baider ◽  
...  

One of the early manifestations of atherosclerotic lesions is endothelial dysfunction developing under conditions of reduced nitric oxide production, hyperhomocysteinemia, and oxidative stress. Bearing in mind high interest shown to gender-specific peculiarities of cardiovascular diseases, it appears important to study the relationship between these features in men and women with stable forms of coronary heart disease (CHD). Material and methods. The study included 102 patients with sable COPD divided into 2 groups (men and women) and 40 practically healthy subjects. Plasma homocysteine levels were measured by high-resolution gas-liquid chromatography with fluorescent detector with the use of Eko-Novo Milikhrom A-02 apparatus (Russia). Standard methods were used to measure plasma lipids, products of their peroxidation (dienic conjugates and products reacting with 2-thibarbituric acid), antioxidant enzymes (glutathioneperoxidase, and superoxide dismutase in erythrocytes), activity of the ceruloplasmin-transferrin system (by electron paramagnetic resonance method), final metabolites of nitric oxide using the Gries reaction. The endothelial function was studies by ultrasound with the evaluation of endothelium-dependent vasodilation. Results. The mean levels of homocystein and final NO metabolites in men with stable CHD were 1.5 times higher (р=0,01) and 12% lower (р = 0,03) than in women. Endothelial dysfunction was more pronounced in men (р< 0,05). Conclusion. Patients with CHD exhibit significant gender-specific differences in blood levels of of homocystein and final NO metabolites as well as in endothelium-dependent vasoreactivity associated with intensification of lipid peroxidation and impairment of antioxidative protection.


2007 ◽  
Vol 13 (4) ◽  
pp. 256-261
Author(s):  
N. YU. Klimenko ◽  
N. V. Drobotya ◽  
A. A. Kastanyan ◽  
V. V. Kaltykova ◽  
E. Sh. Guseynova

A study of daily blood pressure (BP) dynamics, functional endothelial condition at hypertensive patients in combination with tuberculosis of various localization and estimation of an opportunity of correction of the revealed disturbances during 12-week therapy by the fixed combination of perindopril and indapamide - noliprel-forte (Servier, France) were performed. During research more expressed endothelial dysfunction at hypertensive patients, proceeding on a background of tubercular process in comparison with patients with isolated arterial hypertension was revealed. Therapy by noliprel-forte provided the reliable 24-hour control of BP level, which was accompanied by endothelial function normalization that was shown by improvement of a endothelium-dependent vasodilatation and decrease of a von Willebrand factor level. .


2020 ◽  
Vol 26 (30) ◽  
pp. 3684-3699 ◽  
Author(s):  
Nathalie T.B. Delgado ◽  
Wender N. Rouver ◽  
Roger L. dos Santos

Background: Punica granatum L. is an infructescence native of occidental Asia and Mediterranean Europe, popularly referred to as pomegranate. It has been used in ethnomedicine for several applications, including the treatment of obesity, inflammation, diabetes, and the regulation of blood lipid parameters. Thus, pomegranate has been linked to the treatment of cardiovascular diseases that have endothelial dysfunction as a common factor acting mainly against oxidative stress due to its high polyphenol content. Its biocomponents have antihypertensive, antiatherogenic, antihyperglycemic, and anti-inflammatory properties, which promote cardiovascular protection through the improvement of endothelial function. Methods: Different electronic databases were searched in a non-systematic way to uncover the literature of interest. Conclusion: This review article presents updated information on the role of pomegranate in the context of endothelial dysfunction and cardiovascular diseases. We have shown that pomegranate, or rather its components (e.g., tannins, flavonoids, phytoestrogens, anthocyanins, alkaloids, etc.), have beneficial effects on the cardiovascular system, improving parameters such as oxidative stress and the enzymatic antioxidant system, reducing reactive oxygen species formation and acting in an anti-inflammatory way. Thus, this review may contribute to a better understanding of pomegranate's beneficial actions on endothelial function and possibly to the development of strategies associated with conventional treatments of cardiovascular diseases.


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