Cited by 1,957Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

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Endothelial Nitric Oxide Synthase in Vascular Disease: From Marvel to Menace

Förstermann, Ulrich, Münzel, Thomas·2006·Circulation

DOI 10.1161/circulationaha.105.602532

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Abstract

Nitric oxide (NO·) is an important protective molecule in the vasculature, and endothelial NO· synthase (eNOS) is responsible for most of the vascular NO· produced. A functional eNOS oxidizes its substrate l -arginine to l -citrulline and NO·. This normal function of eNOS requires dimerization of the enzyme, the presence of the substrate l -arginine, and the essential cofactor (6 R )-5,6,7,8-tetrahydro- l -biopterin (BH 4 ), one of the most potent naturally occurring reducing agents. Cardiovascular risk factors such as hypertension, hypercholesterolemia, diabetes mellitus, or chronic smoking stimulate the production of reactive oxygen species in the vascular wall. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases represent major sources of this reactive oxygen species and have been found upregulated and activated in animal models of hypertension, diabetes, and sedentary lifestyle and in patients with cardiovascular risk factors. Superoxide (O 2 · − ) reacts avidly with vascular NO· to form peroxynitrite (ONOO − ). The cofactor BH 4 is highly sensitive to oxidation by ONOO − . Diminished levels of BH 4 promote O 2 · − production by eNOS (referred to as eNOS uncoupling). This transformation of eNOS from a protective enzyme to a contributor to oxidative stress has been observed in several in vitro models, in animal models of cardiovascular diseases, and in patients with cardiovascular risk factors. In many cases, supplementation with BH 4 has been shown to correct eNOS dysfunction in animal models and patients. In addition, folic acid and infusions of vitamin C are able to restore eNOS functionality, most probably by enhancing BH 4 levels as well.

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10.1161/res.86.3.347 · DOI
Li H Witte K August M Brausch I Gödtel-Armbrust U Habermeier A Closs EI Oelze M Münzel T Förstermann U. Reversal of eNOS uncoupling and upregulation of eNOS expression lowers blood pressure in hypertensive rats. J Am Coll Cardiol. In press.
10.1161/res.88.2.e14 · DOI
10.1161/circ.99.15.2027 · DOI
10.1161/res.86.5.494 · DOI
10.1161/circ.94.11.2756 · DOI
10.1161/circ.101.11.1261 · DOI
10.1161/circ.100.21.2131 · DOI
10.1161/hyp.30.1.57 · DOI
10.1161/res.77.3.510 · DOI
10.1161/circ.103.9.1282 · DOI
10.1161/hyp.33.6.1353 · DOI
10.1161/res.86.1.e7 · DOI
10.1161/res.86.2.e36 · DOI
10.1161/circ.104.10.1119 · DOI
10.1161/res.87.2.99 · DOI
10.1161/res.87.7.566 · DOI
10.1161/hyp.38.5.1044 · DOI
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10.1161/circ.97.3.237 · DOI
10.1161/atvb.22.1.6 · DOI
10.1161/atvb.20.1.185 · DOI

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Protective Role of S-Nitrosoglutathione (GSNO) Against Cognitive Impairment in Rat Model of Chronic Cerebral Hypoperfusion
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Background
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“Additionally, many cardiovascular disorders have been associated with selective impairment of either eNOS-mediated or IK/SK channel-mediated vasodilatation (Forstermann & Munzel, 2006; Klinger et al. 2013; Ma et al. 2013; Sonkusare et al. 2014; Seki et al. 2017).”
Background
Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase—Implications for Diabetes Progression
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“They usually produce •NO by conversion of the substrate L-arginine to L-citrulline by electron transfer from NADPH and reaction of molecular oxygen with the help of the heme-iron and the cofactor tetrahydrobiopterin (BH4). ucNOS isoforms produce O2•¯ instead of •NO by electron transfer from NADPH to molecular oxygen,…”
Background
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BackgroundInfluential
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Ascorbic Acid Reduces Noise‐Induced Nitric Oxide Production in the Guinea Pig Ear
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Posttranscriptional and transcriptional regulation of endothelial nitric-oxide synthase during hypoxia: the role of microRNAs
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Chronic Co-Administration of Sepiapterin and l -Citrulline Ameliorates Diabetic Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury in Obese Type 2 Diabetic Mice
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Hyperuricemia and the Risk of Heart Failure: Pathophysiology and Therapeutic Implications
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Chemotherapy Induced Cardiotoxicity: A State of the Art Review on General Mechanisms, Prevention, Treatment and Recent Advances in Novel Therapeutics
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Background
Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
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“(2) the requirement for MT1-MMP in NO-”
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CircRNA–miRNA interactions in atherogenesis
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“eNOS must be regarded as both an NO- and an O2 · -producing enzyme, and, therefore, eNOS may have a dual effect on vascular function, depending on its functional state.(7,10,11) Our results provide evidence that the direct action of MNA on the endothelium in the healthy normocholesterolemic and hypercholesterolemic su…”
Background
Activation of NAD(P)H Oxidases by Thromboxane A 2 Receptor Uncouples Endothelial Nitric Oxide Synthase
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Augmented H2S production via cystathionine-beta-synthase upregulation plays a role in pregnancy-associated uterine vasodilation†
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“With these samples we are able to repeat previously reported augmented NOS3 protein expression in human UA during estrogen-dominant physiological states [16].”
BackgroundInfluential
Metallothionein Abrogates GTP Cyclohydrolase I Inhibition–Induced Cardiac Contractile and Morphological Defects
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Caveolin-1 Ablation Reduces the Adverse Cardiovascular Effects of N-ω-Nitro-l-Arginine Methyl Ester and Angiotensin II
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Authors: Förstermann, U., & Münzel, T.
Affiliations: From the Departments of Pharmacology (U.F.) and Internal Medicine II (Cardiology) (T.M.), Johannes Gutenberg University Hospitals, Mainz, Germany.
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2006-04-04
Volume: 113
Issue: 13
Pages: 1708-1714
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/circulationaha.105.602532
OpenAlex: W2146190354
Cited by: 1,957
References: 67
Citations by year: 2026: 93 · 2025: 76 · 2024: 99 · 2023: 86 · 2022: 110 · 2021: 113 · 2020: 110 · 2019: 89 · 2018: 105 · 2017: 105 · 2016: 117 · 2015: 101 · 2014: 123 · 2013: 98 · 2012: 85
FWCI: 62.52
Type: journal article
Language: en
Open access: closed
Locations: Circulation (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 nitric oxide synthase, nitric oxide, tetrahydrobiopterin, eNOS uncoupling, NADPH oxidase, reactive oxygen species, superoxide, peroxynitrite, oxidative stress, cardiovascular risk factors, hypertension, hypercholesterolemia, diabetes mellitus, smoking, folic acid, vitamin C, L-arginine
MeSH terms: Animals, Endothelium, Vascular, Humans, Nitric Oxide, Vascular Diseases, Reactive Oxygen Species, Oxidative Stress, Nitric Oxide Synthase Type III

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Endothelial Nitric Oxide Synthase in Vascular Disease: From Marvel to Menace

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