Cited by 473Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

The DOI matches its Crossref record.

Endothelial Dysfunction in Human Disease

Drexler, Helmut, Hornig, Burkhard·1999·Journal of Molecular and Cellular Cardiology

DOI 10.1006/jmcc.1998.0843

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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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Khaki‐Khatibi, F., Samadi, N., & Yaghoubi, A. (2016) · Journal of Analytical Research in Clinical Medicine · doi:10.15171/jarcm.2016.031 · Cited by 4
Retracted
The Utility of Vascular Dysfunction Studies in the Prediction and Prevention of Preeclampsia: A Historical Review
Matsubara, K., Matsubara, Y., & Ito, M. (2009) · Vascular Disease Prevention · doi:10.2174/1567270000906010163 · Cited by 6
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“The donor endothelial cells are different and present dysfunction in numerous pathological conditions such as atherosclerosis, transplantation or cytomegalovirus infection (Evans et al., 1999; Drexler and Hornig, 1999).”
Background
The Utility of Vascular Dysfunction Studies in the Prediction and Prevention of Preeclampsia: A Historical Review
Matsubara, K., Matsubara, Y., & Ito, M. (2009) · Vascular Disease Prevention · doi:10.2174/1567270001006010163 · Cited by 4
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Retraction Note: Effects of uric acid on endothelial dysfunction in early chronic kidney disease and its mechanisms
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Retracted
Analysis of the Interaction Between Plasmodium falciparum-Infected Erythrocytes and Human Endothelial Cells Using a Laminar Flow System, Bioinformatic Tracking and Transcriptome Analysis
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“Endothelial dysfunction is associated with the major risk factors for atherosclerosis and has been shown to be observed early in the course of atherogenesis, even before structural lesions can be found (Anderson, 1997; Drexler & Hornig, 1999; Verma et al., 2003).”
Background
Positive influence of aspirin on coronary endothelial function: Importance of the dose
Teragawa, H. (2013) · World Journal of Cardiology · doi:10.4330/wjc.v5.i11.426 · Cited by 3
Aging and the Cerebral Microvasculature
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Endothelium‐targeted Gene and Cell‐based Therapy for Cardiovascular Disease
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Human C-peptide is a ligand of the elastin-receptor-complex and therewith central to human vascular remodelling and disease in metabolic syndrome
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Stammzelltherapie nach akutem Myokardinfarkt
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Review on Hypothetical Implementing TGF-β Family Members in Glaucoma Therapy.
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The effects of concurrent hydroalcoholic extract of Amaranthus caudatus L. and Hypericum perforatum L. of fatty streak formation in hypercholesterolemic animals
Kabiri, N. (2011) · African Journal of Pharmacy and Pharmacology · doi:10.5897/ajpp11.476 · Cited by 2
“Statins help nitric oxide synthesis and improve endothelial function (Drexler and Horning, 1999) and (Koh et al., 2000), and inhibit the production of inflammatory cytokines and chemokines, improve autonomic function, and quash myocardial remodeling (Hayashidani et al., 2002); Lefer, 2002).”
Background
Association of an endogenous inhibitor of nitric oxide synthase with cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage
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The Association of Passive Smoking and Serum Urotensin-II Levels in Children
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Subchronic stress effects on vascular reactivity in C57BL/6 strain mice
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Activation of calcium-activated potassium channels by ghrelin: an opportunity to study the (patho)physiological role(s) of endothelium-derived hyperpolarizing factor?
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CORRECTION
(2004) · Postgraduate Medical Journal · doi:10.1136/pgmj.2004.019356corr1 · Cited by 2
From tissue wasting to cachexia: changes in peripheral blood flow and skeletal musculature
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“Endothelial dysfunction can result in impaired tissue perfusion (particularly during stress) and myocardial ischaemia, and may also have adverse long-term effects on vascular remodelling[8].”
Background

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)
DOI: 10.1006/jmcc.1998.0843
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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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Endothelial Dysfunction in Human Disease

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