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Endothelial Dysfunction in Human Disease
Abstract
The vascular endothelium plays a key role in the local regulation of vascular tone by the release of vasodilator substances (i.e. endothelium-derived relaxing factor (EDRF = nitric oxide, NO) and prostacyclin) and vasoconstrictor substances (i.e. thromboxane A2, free radicals, or endothelin). Using either agents like acetylcholine or changes in flow to stimulate the release of EDRF (NO), clinical studies have revealed the importance of EDRF in both basal and stimulated control of vascular tone in large epicardial coronary arteries and in the coronary microcirculation. The regulatory function of the endothelium is altered by cardiovascular risk factors or disorders such as hypercholesterolemia, chronic smoking, hypertension or chronic heart failure. Endothelial dysfunction appears to have detrimental functional consequences as well as adverse longterm effects, including vascular remodelling. Endothelial dysfunction is associated with impaired tissue perfusion particularly during stress and paradoxical vasoconstriction of large conduit vessels including the coronary arteries. These effects may cause or contribute to myocardial ischemia. Several mechanisms may be involved in the development of endothelial dysfunction, such as reduced synthesis and release of EDRF or enhanced inactivation of EDRF after its release from endothelial cells by radicals or oxidized low-density lipoprotein (LDL). Increased plasma levels of oxidized LDL have been noted in chronic smokers and are related to the extent endothelial dysfunction, raising the possibility that chronic smoking potentiates endothelial dysfunction by increasing circulating and tissue levels of oxidized LDL. In heart failure, cytokines and/or reduced flow (reflecting reduced shear stress) may be involved in the development of endothelial dysfunction and can be reversed by physical training. Other mechanisms include an activated renin-angiotensin system (i.e. postmyocardial infarction) with increased breakdown of bradykinin by enhanced angiotensin converting enzyme (ACE) activity. There is evidence that endogenous bradykinin is involved in coronary vasomotor control both in coronary conduit and resistance vessels. ACE inhibitors enhance endothelial function by a bradykinin-dependent mechanism and probably also by blunting the generation of superoxide anion. Endothelial dysfunction appears to be reversible by administering L-arginine, the precursor of nitric oxide, lowering cholesterol levels, physical training, antioxidants such as vitamin C, or ACE inhibition.
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“A few studies have found inhibitory effects of dietary nitrate on platelet aggregation, suggesting that inhibition of abnormal platelet aggregation may be partly responsible for the cardiovascular benefits of nitrate supplementation.”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [106]
In the citing paper
“For example, Richardson et al. (106) demonstrated that a single 2 mmol bolus of potassium nitrate inhibited platelet aggregation by up to 31 % in healthy individuals.”
From The effects of dietary nitrate on blood pressure and endothelial function: a review of human intervention studies (2013) · cites this paper as [106]
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Nitrotyrosine Causes Selective Vascular Endothelial Dysfunction and DNA Damage
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Trends of tea in cardiovascular health and disease: A critical review
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Vascular Reactivity in Hypogonadal Men Is Reduced by Androgen Substitution
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Metadata
- Authors
- Drexler, H., & Hornig, B.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 1999-01
- Volume
- 31
- Issue
- 1
- Pages
- 51-60
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2074957886
- Cited by
- 471
- References
- 0
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 3 · 2023: 5 · 2022: 8 · 2021: 4 · 2020: 7 · 2019: 11 · 2018: 4 · 2017: 7 · 2016: 14 · 2015: 11 · 2014: 18 · 2013: 23 · 2012: 19
- FWCI
- 16.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Molecular and Cellular Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- endothelial dysfunction, nitric oxide, endothelium-derived relaxing factor, coronary microcirculation, oxidized LDL, chronic smoking, heart failure, renin-angiotensin system, bradykinin, ACE inhibitors, L-arginine, exercise training, antioxidants, myocardial ischemia, vascular remodeling, shear stress, hypertension, hypercholesterolemia
- MeSH terms
- Acetylcholine, Ascorbic Acid, Cardiac Output, Low, Coronary Disease, Dose-Response Relationship, Drug, Endothelium, Vascular, Enzyme Inhibitors, Humans, Hypercholesterolemia, Hyperemia, Lipoproteins, LDL, Radial Artery, omega-N-Methylarginine
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