Asymmetric Dimethylarginine (ADMA): A Novel Risk Factor for Endothelial Dysfunction: Its Role in Hypercholesterolemia
Abstract
Background —Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide (NO) synthase. Because endothelial NO elaboration is impaired in hypercholesterolemia, we investigated whether plasma concentrations of ADMA are elevated in young, clinically asymptomatic hypercholesterolemic adults. We further studied whether such elevation of ADMA levels was correlated with impaired endothelium-dependent, NO-mediated vasodilation and urinary nitrate excretion. In a randomized, double-blind, placebo-controlled study, we investigated whether these changes could be reversed with exogenous l -arginine. Methods and Results —We measured plasma levels of l -arginine, ADMA, and symmetrical dimethylarginine (SDMA) by high-performance liquid chromatography in 49 hypercholesterolemic (HC) and 31 normocholesterolemic (NC) humans. In 8 HC subjects, endothelium-dependent forearm vasodilation was assessed before and after an intravenous infusion of l -arginine or placebo and compared with 8 NC control subjects. ADMA levels were significantly elevated by >100% (2.17±0.15 versus 1.03±0.09 μmol/L; P <0.05) in HC subjects compared with NC adults. l -Arginine levels were similar, resulting in a significantly decreased l -arginine/ADMA ratio in HC subjects (27.7±2.4 versus 55.7±5.4; P <0.05). In 8 HC subjects, intravenous infusion of l -arginine significantly increased the l -arginine/ADMA ratio and normalized endothelium-dependent vasodilation and urinary nitrate excretion. ADMA levels were inversely correlated with endothelium-mediated vasodilation ( R =0.762, P <0.01) and urinary nitrate excretion rates ( R =0.534, P <0.01). Conclusions —We find that ADMA is elevated in young HC individuals. Elevation of ADMA is associated with impaired endothelium-dependent vasodilation and reduced urinary nitrate excretion. This abnormality is reversed by administration of l -arginine. ADMA may be a novel risk factor for endothelial dysfunction in humans.
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Individuals with atherosclerosis, chronic heart failure, hypertension, hypercholesterolemia, and diabetes mellitus, as well as women with PCOS, exhibit elevated levels of ADMA.
“Studies have demonstrated that individuals with atherosclerosis, chronic heart failure [16, 17], hypertension [18], hypercholesterolemia [19], and diabetes mellitus [20], as well as women with PCOS [21], exhibit elevated levels of ADMA [22].”
From Association of dietary phytochemical index with metabolic markers, serum asymmetric dimethylarginine and atherogenic indices in patients with polycystic ovary syndrome (2025) · cites this paper as [19]
The Baseline Plasma L-Arginine and Dimethylarginine Concentrations section (page unavailable) reports significantly higher ADMA in hypercholesterolemic subjects than in controls. The Subjects section says participants had no signs of atherosclerotic vascular disease and that those with diabetes were excluded. The Discussion mentions a correlation with peripheral arterial disease severity, but the copy does not establish elevated ADMA across the other listed conditions or in women with PCOS. (LLM, conf=0.90)
Experimental — accuracy not yet measuredAvailability of l-arginine may be jeopardized under endothelial dysfunction, and concentrations of inhibitory l-arginine metabolites such as ADMA can increase in pathological conditions.
“Several lines of evidence indicate that the availability of l-arginine may be jeopardized under endothelial dysfunction, and the concentrations of inhibitory l-arginine metabolites, such as ADMA, can also increase in pathological conditions (107, 1053).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [107]
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“Studies have demonstrated that individuals with atherosclerosis, chronic heart failure [16, 17], hypertension [18], hypercholesterolemia [19], and diabetes mellitus [20], as well as women with PCOS [21], exhibit elevated levels of ADMA [22].”
- Authors
- Böger, R. H., Bode-Böger, S. M., Szuba, A., Tsao, P. S., Chan, J. R., Tangphao, O., Blaschke, T. F., & Cooke, J. P.
- Affiliations
- From the Divisions of Cardiovascular Medicine (R.H.B., S.M.B.-B., P.S.T., J.R.C., J.P.C.) and Clinical Pharmacology (O.T., T.F.B.), Stanford University School of Medicine, Stanford, Calif, and Department of Angiology (A.S.), Jaegellonian University, Wroclaw, Poland.
- Stanford Medicine (US)
- Venue
- Circulation
- Published
- 1998-11-03
- Volume
- 98
- Issue
- 18
- Pages
- 1842-1847
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2106478344
- Cited by
- 1,181
- References
- 47
- Citations by year
- 2026: 7 · 2025: 18 · 2024: 21 · 2023: 24 · 2022: 19 · 2021: 24 · 2020: 25 · 2019: 26 · 2018: 25 · 2017: 38 · 2016: 36 · 2015: 42 · 2014: 38 · 2013: 45 · 2012: 57
- FWCI
- 16.97
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- Deutsche Forschungsgemeinschaft
- Boehringer Ingelheim Stiftung
- National Institutes of Health (5f32hl008779-02)
- National Heart, Lung, and Blood Institute (1F32-HL-08779, 1R01-HL58638)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer-related gene regulation
- Keywords
- asymmetric dimethylarginine, endothelial dysfunction, hypercholesterolemia, nitric oxide synthase inhibition, nitric oxide, L-arginine, endothelium-dependent vasodilation, urinary nitrate excretion, symmetric dimethylarginine, L-arginine/ADMA ratio, risk factors
- MeSH terms
- Arginine, Double-Blind Method, Endothelium, Vascular, Female, Humans, Hypercholesterolemia, Injections, Intravenous, Male, Middle Aged, Osmolar Concentration, Risk Factors, Nitric Oxide Synthase, Nitric Oxide Synthase Type III
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