scholarly journals Endothelin-1 contributes to endothelial dysfunction and enhanced vasoconstriction through augmented superoxide production in penile arteries from insulin-resistant obese rats: role of ETAand ETBreceptors

2014 ◽  
Vol 171 (24) ◽  
pp. 5682-5695 ◽  
Author(s):  
A Sánchez ◽  
P Martínez ◽  
M Muñoz ◽  
S Benedito ◽  
A García-Sacristán ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Superoxide Production ◽  
Endothelin 1 ◽  
Insulin Resistant ◽  
Obese Rats ◽  
Penile Arteries

scholarly journals Role of Neural NO Synthase (nNOS) Uncoupling in the Dysfunctional Nitrergic Vasorelaxation of Penile Arteries from Insulin-Resistant Obese Zucker Rats

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e36027 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
María Pilar Martínez ◽  
Belén Climent ◽  
Sara Benedito ◽  
...  
Keyword(s):  
No Synthase ◽  
Zucker Rats ◽  
Insulin Resistant ◽  
Obese Zucker Rats ◽  
Penile Arteries

scholarly journals The Role of Endothelial Dysfunction in the Development of Cardiotoxic Action of Cytostatics in Patients with Lymphoproliferative Diseases

Kardiologiia ◽  
2019 ◽  
Vol 59 (4) ◽  
pp. 64-66 ◽  
Author(s):  
D. A. Budanova ◽  
Yu. N. Belenkov ◽  
I. Ya. Sokolova ◽  
O. N. Antyufeeva ◽  
V. I. Ershov ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Normal Values ◽  
Clear Understanding ◽  
Age Group ◽  
Lymphoproliferative Diseases ◽  
Endothelin 1 ◽  
Vasoconstrictor Effect ◽  
Before And After ◽  
Chemotherapy Cardiotoxicity

Understanding mechanisms of chemotherapy cardiotoxicity is an important problem due to the lack of clear understanding of its occurrence. Development of endothelial dysfunction is considered to be one of possible ways in implementation of these side effects. The analysis of endothelin-1 and e-selectin levels in 26  patients with lymphoproliferative diseases before and after the completion of the treatment program was been performed. The results of the study showed normal values of E-selectin level and increased level of endothelin-1 in the whole group of patients before treatment. After completion of chemotherapy program, in the whole group, there was a decrease of these two markers. However, values of level of endothelin-1 with vasoconstrictor effect remained high even after the end of therapy. It is imp ortant that at detailed analysis the dynamics of investigated markers in patients of older age group (median age 64 years) was associated with worsening of endothelial dysfunction.

Role of Endothelin-1 and Endothelial Dysfunction in Prehypertension

2012 ◽  
Vol 28 (3) ◽  
pp. 251-253 ◽  
Author(s):  
Christine K. Kissel ◽  
Todd J. Anderson
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelin 1

Quercetin inhibits vascular superoxide production induced by endothelin-1: Role of NADPH oxidase, uncoupled eNOS and PKC

2009 ◽  
Vol 202 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Miguel Romero ◽  
Rosario Jiménez ◽  
Manuel Sánchez ◽  
Rocío López-Sepúlveda ◽  
Maria José Zarzuelo ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Superoxide Production ◽  
Endothelin 1

scholarly journals Oral nicotine aggravates endothelial dysfunction and vascular inflammation in diet-induced obese rats: Role of macrophage TNFα

PLoS ONE ◽  
2017 ◽  
Vol 12 (12) ◽  
pp. e0188439 ◽  
Author(s):  
Chang Liu ◽  
Ming-Sheng Zhou ◽  
Yao Li ◽  
Aimei Wang ◽  
Kiranmai Chadipiralla ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Vascular Inflammation ◽  
Obese Rats ◽  
Oral Nicotine

The interaction between endothelin-1 and nitric oxide in the vasculature: new perspectives

2011 ◽  
Vol 300 (6) ◽  
pp. R1288-R1295 ◽  
Author(s):  
Stephane L. Bourque ◽  
Sandra T. Davidge ◽  
Michael A. Adams
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Vascular Remodeling ◽  
Vascular Function ◽  
No Synthase ◽  
Endothelin 1 ◽  
No Signaling ◽  
No Bioavailability

Nitric oxide (NO) and endothelin-1 (ET-1) are natural counterparts in vascular function, and it is becoming increasingly clear that an imbalance between these two mediators is a characteristic of endothelial dysfunction and is important in the progression of vascular disease. Here, we review classical and more recent data that suggest that ET-1 should be regarded as an essential component of NO signaling. In particular, we review evidence of the role of ET-1 in models of acute and chronic NO synthase blockade. Furthermore, we discuss the possible mechanisms by which NO modulates ET-1 activity. On the basis of these studies, we suggest that NO tonically inhibits ET-1 function, and in conditions of diminished NO bioavailability, the deleterious effects of unmitigated ET-1 actions result in vasoconstriction and eventually lead to vascular remodeling and dysfunction.

Anthracycline-Induced Cardiotoxicity: The Role of Endothelial Dysfunction

Cardiology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Elena V. Grakova ◽  
Sergey N. Shilov ◽  
Kristina V. Kopeva ◽  
Ekaterina N. Berezikova ◽  
Anna A. Popova ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Genetic Factors ◽  
Vascular Toxicity ◽  
Endothelin 1 ◽  
Endothelial Cell Death ◽  
Endothelial Nitric Oxide ◽  
Genetic Susceptibility Factor

Cardiovascular disease remains the leading cause of mortality accounting up to 40% of all deaths, but, currently, cancer is prominent cause of death globally. Anthracyclines are the cornerstone of chemotherapy in women with breast cancer. However, its clinical use is limited by their cardiotoxic effects that can trigger heart failure development. Vascular toxicity of chemotherapy may be linked with endothelial dysfunction because anthracycline damage of endothelial cells can lead to the development and progression of cardiomyopathy by decreasing the release and activity of endothelial factors and, ultimately, endothelial cell death. These processes suppress anti-inflammatory and vascular reparative functions and initiate the development of future cardiovascular events. Recent studies have shown that chemotherapy may induce toxicity in the vascular endothelium and is accompanied by systemic endothelial dysfunction in patients with diagnosed cardiovascular diseases. Because the initial endothelial cell insult is likely asymptomatic, there is often a long delay between the termination of doxorubicin therapy and the onset of vascular disorders. In this case, genetic susceptibility factor will help to identify susceptible patients in the future. The objectives of this study were to evaluate prognostic role of molecular (endothelin-1) and genetic factors (gene polymorphisms of endothelial nitric oxide (NO) synthase (NOS3, rs1799983), endothelin-1 receptor type A (EDNRA, C+70G, rs5335) and NADPH oxidase (C242T, rs4673) in development of endothelial dysfunction and anthracycline-induced cardiotoxicity in women without cardiovascular diseases.

scholarly journals The Causal Relationship between Endothelin-1 and Hypertension: Focusing on Endothelial Dysfunction, Arterial Stiffness, Vascular Remodeling, and Blood Pressure Regulation

Life ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 986
Author(s):  
Krasimir Kostov
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Arterial Stiffness ◽  
Structural Changes ◽  
Vascular Wall ◽  
Low Grade ◽  
Endothelin 1 ◽  
Vascular Regulation ◽  
Wide Range

Hypertension (HTN) is one of the most prevalent diseases worldwide and is among the most important risk factors for cardiovascular and cerebrovascular complications. It is currently thought to be the result of disturbances in a number of neural, renal, hormonal, and vascular mechanisms regulating blood pressure (BP), so crucial importance is given to the imbalance of a number of vasoactive factors produced by the endothelium. Decreased nitric oxide production and increased production of endothelin-1 (ET-1) in the vascular wall may promote oxidative stress and low-grade inflammation, with the development of endothelial dysfunction (ED) and increased vasoconstrictor activity. Increased ET-1 production can contribute to arterial aging and the development of atherosclerotic changes, which are associated with increased arterial stiffness and manifestation of isolated systolic HTN. In addition, ET-1 is involved in the complex regulation of BP through synergistic interactions with angiotensin II, regulates the production of catecholamines and sympathetic activity, affects renal hemodynamics and water–salt balance, and regulates baroreceptor activity and myocardial contractility. This review focuses on the relationship between ET-1 and HTN and in particular on the key role of ET-1 in the pathogenesis of ED, arterial structural changes, and impaired vascular regulation of BP. The information presented includes basic concepts on the role of ET-1 in the pathogenesis of HTN without going into detailed analyses, which allows it to be used by a wide range of specialists. Also, the main pathological processes and mechanisms are richly illustrated for better understanding.

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