scholarly journals Endothelial function and its role in the formation of cardiovascular pathology in patients with rheumatoid arthritis

2019 ◽  
Vol 100 (3) ◽  
pp. 451-456
Author(s):  
A A Tulichev ◽  
N Yu Borovkova ◽  
N N Borovkov ◽  
A A Spassky ◽  
I V Polyakova ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Unknown Origin ◽  
Vascular Wall ◽  
Cardiovascular Complications ◽  
Point Of View ◽  
Microvascular Changes ◽  
Initial Stage

Currently rheumatoid arthritis is considered as an immune inflammatory disease of unknown origin characterized by chronic erosive arthritis and systemic damage of internal organs, leading to early disability and reduced life expectancy. Cardiovascular diseases are most often mentioned as factors of poor prognosis in rheumatoid arthritis. Pathology of the cardiovascular system in rheumatoid arthritis is usually associated with the macro- and microvascular changes and rheumatoid lesions of the heart. The leading factor in the damage of the vascular wall in rheumatoid arthritis is systemic inflammation affecting its viscosity and elastic properties, increased rigidity, impaired endothelial function. Endothelial dysfunction is currently regarded to as an initial stage of morphogenesis of various vascular disorders. It is considered as a subclinical marker of cardiovascular diseases and the earliest predictor of cardiovascular complications. From this point of view study of endothelial dysfunction in patients with rheumatoid arthritis aimed at determining cardiovascular risk is a perspective direction. Only single and fragmentary information about certain endothelial functions in patients with rheumatoid arthritis and substances released in this. There is no clear analysis of relationship between them and dependence on the process activity. Not clear is their role in the pathology of the vascular wall in rheumatoid arthritis. This literature review discusses the problem of endothelial dysfunction in rheumatoid arthritis patients as well as its role in the development of cardiovascular diseases in these patients. The development mechanisms and the role of immune inflammation in its formation are considered. Also the association was found between chronic inflammatory activity indicators in rheumatoid arthritis and various biological markers and development of endothelial dysfunction. The effects of antirheumatic treatment on endothelial dysfunction in these patients were analyzed.

scholarly journals Crossing the Vascular Wall: Common and Unique Mechanisms Exploited by Different Leukocyte Subsets during Extravasation

2015 ◽  
Vol 2015 ◽  
pp. 1-23 ◽  
Author(s):  
Michael Schnoor ◽  
Pilar Alcaide ◽  
Mathieu-Benoit Voisin ◽  
Jaap D. van Buul
Keyword(s):  
Rheumatoid Arthritis ◽  
Current Knowledge ◽  
Leukocyte Adhesion ◽  
Vascular Wall ◽  
Point Of View ◽  
Regulatory Mechanisms ◽  
Integrin Receptors ◽  
Endothelial Monolayers ◽  
Leukocyte Extravasation ◽  
Endothelial Adhesion Molecules

Leukocyte extravasation is one of the essential and first steps during the initiation of inflammation. Therefore, a better understanding of the key molecules that regulate this process may help to develop novel therapeutics for treatment of inflammation-based diseases such as atherosclerosis or rheumatoid arthritis. The endothelial adhesion molecules ICAM-1 and VCAM-1 are known as the central mediators of leukocyte adhesion to and transmigration across the endothelium. Engagement of these molecules by their leukocyte integrin receptors initiates the activation of several signaling pathways within both leukocytes and endothelium. Several of such events have been described to occur during transendothelial migration of all leukocyte subsets, whereas other mechanisms are known only for a single leukocyte subset. Here, we summarize current knowledge on regulatory mechanisms of leukocyte extravasation from a leukocyte and endothelial point of view, respectively. Specifically, we will focus on highlighting common and unique mechanisms that specific leukocyte subsets exploit to succeed in crossing endothelial monolayers.

scholarly journals Pentaerythritol Tetranitrate In Vivo Treatment Improves Oxidative Stress and Vascular Dysfunction by Suppression of Endothelin-1 Signaling in Monocrotaline-Induced Pulmonary Hypertension

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Sebastian Steven ◽  
Matthias Oelze ◽  
Moritz Brandt ◽  
Elisabeth Ullmann ◽  
Swenja Kröller-Schön ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Hypertension ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Whole Blood ◽  
Pulmonary Arteries ◽  
Vascular Wall ◽  
Pentaerythritol Tetranitrate ◽  
Endothelin 1 ◽  
Pulmonary Arterial

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.

scholarly journals Endothelial function in normal and pathological conditions

2019 ◽  
pp. 154-159
Author(s):  
A. V. Pizov ◽  
N. A. Pizov ◽  
O. A. Skachkova ◽  
N. V. Pizovа
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Tone ◽  
Vascular Wall ◽  
The State ◽  
Vascular Growth ◽  
Pathological Conditions ◽  
Basic Functions

The article presents the data on the state of endothelial function in the normally and in various diseases and conditions. The basic  functions of endothelium in modulation of vascular tone, atrombogenicity and thrombogenicity of the vascular wall, regulation of  vascular wall adhesion, regulation of vascular growth are described. The main causes leading to the formation of endothelial  dysfunction and the mechanisms underlying it are highlighted. Numerous studies on the evaluation of endothelial function in  various diseases are presented. The basic methods of drug and non-drug correction of endothelial dysfunction are presented. 

Protective Effects of Pomegranate in Endothelial Dysfunction

2020 ◽  
Vol 26 (30) ◽  
pp. 3684-3699 ◽  
Author(s):  
Nathalie T.B. Delgado ◽  
Wender N. Rouver ◽  
Roger L. dos Santos
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Common Factor ◽  
Blood Lipid ◽  
Punica Granatum ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Anti Inflammatory

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.

Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase

2010 ◽  
Vol 120 (8) ◽  
pp. 321-333 ◽  
Author(s):  
Rocío López-Sepúlveda ◽  
Manuel Gómez-Guzmán ◽  
Maria José Zarzuelo ◽  
Miguel Romero ◽  
Manuel Sánchez ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Endothelial Function ◽  
Oxidase Activity ◽  
Red Wine ◽  
Vascular Wall ◽  
Nadph Oxidase Activity ◽  
Wine Polyphenols ◽  
Red Wine Polyphenols ◽  
O2 Production

RWPs (red wine polyphenols) exert antihypertensive effects and improve endothelial function by reducing the plasma levels of ET-1 (endothelin-1) and the subsequent vascular production of O2•− (superoxide anion). Our present study was designed to evaluate whether RWPs act directly in the vascular wall improving endothelial dysfunction and O2•− production induced by ET-1 and to analyse the compounds responsible for these protective effects. We incubated rat isolated aortic rings in the presence or absence of ET-1 (10 nM) and RWPs (10−4 to 10−2 g/l) or catechin (0.2 μM), epicatechin (10 μM) and resveratrol (0.1 μM). ET-1 reduced the relaxant responses to acetylcholine, increased intracellular O2•− production, NADPH oxidase activity and protein expression of NADPH oxidase subunit p47phox. All these changes were prevented by RWPs. The preventive effects of RWPs were unaffected by co-incubation with either ICI-182780, an ER (oestrogen receptor) antagonist, or GW9662, a PPARγ (peroxisome-proliferator-activated receptor γ) antagonist. RWPs inhibited the phosphorylation of the mitogen-activated protein kinase, ERK1/2 (extracellular signal-regulated kinase 1/2), a key regulator of p47phox expression in response to ET-1. When the isolated polyphenols were tested, at the concentrations found in 10−2 g/l RWPs, only epicatechin prevented endothelial dysfunction and all biochemical changes induced by ET-1 in the vascular wall. Taken together, these results indicate that RWPs prevent ET-1-induced vascular O2•− production by reducing overexpression of p47phox and the subsequent increased NADPH oxidase activity, leading to improvement in endothelial function. The effects of RWPs appear to be independent of ER and PPARγ activation and are related to ERK1/2 inhibition.

scholarly journals Dynamin-related protein 1 mediates low glucose-induced endothelial dysfunction in human arterioles

2017 ◽  
Vol 312 (3) ◽  
pp. H515-H527 ◽  
Author(s):  
Michael J. Tanner ◽  
Jingli Wang ◽  
Rong Ying ◽  
Tisha B. Suboc ◽  
Mobin Malik ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Cardiovascular Complications ◽  
Mitochondrial Morphology ◽  
Vascular Relaxation ◽  
Mitochondrial Fragmentation ◽  
Low Glucose

Intensive glycemic regulation has resulted in an increased incidence of hypoglycemia. Hypoglycemic burden correlates with adverse cardiovascular complications and contributes acutely and chronically to endothelial dysfunction. Prior data indicate that mitochondrial dysfunction contributes to hypoglycemia-induced endothelial dysfunction, but the mechanisms behind this linkage remain unknown. We attempt to determine whether clinically relevant low-glucose (LG) exposures acutely induce endothelial dysfunction through activation of the mitochondrial fission process. Characterization of mitochondrial morphology was carried out in cultured endothelial cells by using confocal microscopy. Isolated human arterioles were used to explore the effect LG-induced mitochondrial fission has on the formation of detrimental reactive oxygen species (ROS), bioavailability of nitric oxide (NO), and endothelial-dependent vascular relaxation. Fluorescence microscopy was employed to visualize changes in mitochondrial ROS and NO levels and videomicroscopy applied to measure vasodilation response. Pharmacological disruption of the profission protein Drp1 with Mdivi-1 during LG exposure reduced mitochondrial fragmentation among vascular endothelial cells (LG: 0.469; LG+Mdivi-1: 0.276; P = 0.003), prevented formation of vascular ROS (LG: 2.036; LG+Mdivi-1: 1.774; P = 0.005), increased the presence of NO (LG: 1.352; LG+Mdivi-1: 1.502; P = 0.048), and improved vascular dilation response to acetylcholine (LG: 31.6%; LG+Mdivi-1; 78.5% at maximum dose; P < 0.001). Additionally, decreased expression of Drp1 via siRNA knockdown during LG conditions also improved vascular relaxation. Exposure to LG imparts endothelial dysfunction coupled with altered mitochondrial phenotypes among isolated human arterioles. Disruption of Drp1 and subsequent mitochondrial fragmentation events prevents impaired vascular dilation, restores mitochondrial phenotype, and implicates mitochondrial fission as a primary mediator of LG-induced endothelial dysfunction. NEW & NOTEWORTHY Acute low-glucose exposure induces mitochondrial fragmentation in endothelial cells via Drp1 and is associated with impaired endothelial function in human arterioles. Targeting of Drp1 prevents fragmentation, improves vasofunction, and may provide a therapeutic target for improving cardiovascular complications among diabetics. Listen to this article’s corresponding podcast @ http://ajpheart.podbean.com/e/mitochondrial-dynamics-impact-endothelial-function/ .

scholarly journals ENDOTHELIAL DYSFUNCTION AS PREDICTOR OF SUBCLINICAL AND MANIFEST ATHEROSCLEROSIS

2018 ◽  
Vol 3 (3) ◽  
pp. 39-46
Author(s):  
OV V Fatenkov ◽  
VV V Simerzin ◽  
IV V Gagloeva ◽  
MA A Galkina ◽  
YaA A Panisheva ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Angiotensin Converting Enzyme ◽  
Endothelial Function ◽  
Calcium Antagonists ◽  
Converting Enzyme ◽  
Atherosclerotic Cardiovascular Diseases

This survey presents the role of endothelial dysfunction in pathogenesis of atherosclerotic cardiovascular diseases as predictor of their development. Leading risk factors of endothelial dysfunction and methods of its diagnostics are also shown. Special attention is given to non medicamental correction of endothelial function disorders and its pharmacotherapy with statins, inhibitors of angiotensin converting enzyme (ACE), calcium antagonists and other drugs.

scholarly journals Differential Associations of Inflammatory and Endothelial Biomarkers with Disease Activity in Rheumatoid Arthritis of Short Duration

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Ewa Klimek ◽  
Anna Skalska ◽  
Beata Kwaśny-Krochin ◽  
Andrzej Surdacki ◽  
Joanna Sulicka ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Endothelial Dysfunction ◽  
Disease Activity ◽  
Short Duration ◽  
High Sensitivity ◽  
Vascular Wall ◽  
Endothelial Activation ◽  
High Disease Activity ◽  
Inflammatory Reactions ◽  
Chemotactic Protein

Objectives. To estimate endothelial dysfunction in patients with rheumatoid arthritis (RA) of short duration in relation to disease activity based on the assessment of 28 joints (DAS28).Methods. We studied 29 patients (22 women, mean age 41 (SD, 9) years) with RA of short duration and 29 healthy controls. The RA subjects were divided into those with low (DAS28: 2.6–5.1,n=18) or high (DAS28>5.1,n=11) disease activity. Exclusion criteria included clinically overt atherosclerosis and other coexistent diseases. Biochemical markers of inflammatory activation and endothelial dysfunction were measured.Results. There were no significant intergroup differences in the majority of classical cardiovascular risk factors. High-sensitivity C-reactive protein, tumor necrosis factor-α, and interleukin-6 were increased in RA subjects. Compared to the controls, levels of soluble vascular cell adhesion molecule-1, von Willebrand factor, and pentraxin-3 were significantly elevated in RA subjects with low disease activity, exhibiting no further significant rises in those with high disease activity. Asymmetric dimethyl-L-arginine, soluble E-selectin, monocyte chemotactic protein-1, and osteoprotegerin were increased only in RA patients with high disease activity.Conclusions. Our findings might suggest a dissociation of pathways governing generalized and joint-specific inflammatory reactions from those involved in endothelial activation and inflammation within the vascular wall.

Hyperglycemia and hyperlipidemia are associated with endothelial dysfunction during the development of type 2 diabetes

2007 ◽  
Vol 85 (5) ◽  
pp. 562-567 ◽  
Author(s):  
Elena B. Okon ◽  
Ada W.Y. Chung ◽  
Hongbin Zhang ◽  
Ismail Laher ◽  
Cornelis van Breemen
Keyword(s):  
Type 2 Diabetes ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Plasma Levels ◽  
Early Stage ◽  
Cardiovascular Complications ◽  
Older Age ◽  
Metabolic Markers

Diabetes mellitus impairs endothelial function, which can be considered as the hallmark in the development of cardiovascular diseases. Hyperglycemia, hyperinsulinemia, and hyperlipidemia are believed to contribute to endothelial dysfunction. In the present study, we investigated the possible links among these plasma metabolic markers and endothelial function in a mouse model during the development of type 2 diabetes. C57BL/6J-Lepob/ob mice at 8, 12, and 16 weeks were used to study endothelial function during the establishment of type 2 diabetes. Endothelial function was accessed in vitro in the thoracic aorta by measuring acetylcholine (ACh)-stimulated vasodilatation. Blood plasma was obtained for the measurements of glucose, insulin, triglycerides, and cholesterol levels. Correlation and multiple regression analysis revealed strong negative associations between the ACh responsiveness and the plasma levels of glucose, insulin, and lipid profiles at the age of 8 weeks. Associations were observed at neither older age nor in C57BL/6J mice. In conclusion, the increase in plasma levels of glucose, insulin, and lipids is associated with the impairment of the endothelial function during the early stage of the development of type 2 diabetes. The loss of correlation at an older age suggests multifactorial regulation of endothelial function and cardiovascular complications at later stages of the disease.

scholarly journals Effect of Different Classes of Antihypertensive Drugs on Endothelial Function and Inflammation

2019 ◽  
Vol 20 (14) ◽  
pp. 3458 ◽  
Author(s):  
Isabella Viana Gomes Silva ◽  
Roberta Carvalho de Figueiredo ◽  
Danyelle Romana Alves Rios
Keyword(s):  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Antihypertensive Drugs ◽  
Vascular Inflammation ◽  
Functional Changes ◽  
Beneficial Effects ◽  
Reactive Protein ◽  
Pressure Lowering ◽  
Effect Of Treatment

Hypertension is characterized by structural and functional changes in blood vessels that travel with increased arterial stiffness, vascular inflammation, and endothelial dysfunction. Some antihypertensive drugs have been shown to improve endothelial function and reduce levels of inflammatory markers regardless of the effect of blood pressure lowering. Third-generation β-blockers, such as nebivolol and carvedilol, because they have additional properties, have been shown to improve endothelial function in patients with hypertension. Calcium channel antagonists, because they have antioxidant effects, may improve endothelial function and vascular inflammation.The Angiotensin Receptor Blocker (ARBs) are able to improve endothelial dysfunction and vascular inflammation in patients with hypertension and other cardiovascular diseases. Angiotensin converting enzyme (ACE) inhibitors have shown beneficial effects on endothelial function in patients with hypertension and other cardiovascular diseases, however there are few studies evaluating the effect of treatment with this class on the reduction of C-reactive protein (CRP) levels. Further studies are needed to assess whether treatment of endothelial dysfunction and vascular inflammation may improve the prognosis of patients with essential hypertension.

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