Angiotensin Converting Enzyme Inhibition and Angiotensin II AT1-Receptor Blockade Reduce the Levels of Asymmetrical NG, NG-Dimethylarginine in Human Essential Hypertension*
TLDR
Levels of ADMA were reduced with enalapril and eprosartan therapy, suggesting a specific action of these drugs on ADMA levels that is independent of BP.About:
This article is published in American Journal of Hypertension.The article was published on 2002-07-01 and is currently open access. It has received 139 citations till now. The article focuses on the topics: Enalapril & Eprosartan.read more
Citations
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Endothelial function and oxidative stress in cardiovascular diseases.
TL;DR: This review focuses on recent findings and interaction between endothelium-dependent vasodilation and oxidative stress in cardiovascular diseases.
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ADMA and oxidative stress
Karsten Sydow,Thomas Münzel +1 more
TL;DR: Elevated plasma concentrations of the endogenous nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) represent a novel risk factor for the development of endothelial dysfunction and a predictor for all-cause and cardiovascular mortality.
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Asymmetrical dimethylarginine: the Uber marker?
TL;DR: A burgeoning body of literature is examined that supports ADMA as an “Uber marker,” a biochemical factor mediating the adverse vascular effects of many other risk factors and markers that are associated with endothelial vasodilator dysfunction.
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The emerging role of asymmetric dimethylarginine as a novel cardiovascular risk factor
TL;DR: The administration of L-arginine has been shown to improve endothelium-dependent vascular function in subjects with high ADMA levels, and is becoming a goal for pharmacotherapeutic intervention.
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The Role of Asymmetric Dimethylarginine (ADMA) in Endothelial Dysfunction and Cardiovascular Disease
TL;DR: Interventions such as treatment with L-arginine have been shown to improve endothelium-mediated vasodilatation in people with high ADMA levels, however the clinical utility of modifying circulating ADma levels remains uncertain.
References
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Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure.
TL;DR: In-vitro and in-vivo evidence that NO synthesis can be inhibited by an endogenous compound, NG,NG-dimethylarginine, ADMA is described, which might contribute to the hypertension and immune dysfunction associated with chronic renal failure.
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Novel mechanism for endothelial dysfunction: dysregulation of dimethylarginine dimethylaminohydrolase.
TL;DR: The results suggest that the endothelial vasodilator dysfunction observed in hypercholesterolemia may be due to reduced degradation of ADMA, the endogenous inhibitor of NOS.
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Does ADMA cause endothelial dysfunction
TL;DR: Plasma levels of this inhibitor of nitric oxide synthase are elevated in patients with atherosclerosis and in those with risk factors for Atherosclerosis, suggesting that ADMA may be a novel risk factor for vascular disease.
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LDL cholesterol upregulates synthesis of asymmetrical dimethylarginine in human endothelial cells: involvement of S-adenosylmethionine-dependent methyltransferases.
Rainer H. Böger,Karsten Sydow,Jürgen Borlak,Thomas Thum,Henrike Lenzen,Bibiana Schubert,Dimitrios Tsikas,Stefanie M. Bode-Böger +7 more
TL;DR: The data suggest that the production of ADMA by human endothelial cells is regulated by S-adenosylmethionine-dependent methyltransferases, which may be due in part to the enhanced gene expression of PRMTs.
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Acute and Chronic Angiotensin-1 Receptor Antagonism Reverses Endothelial Dysfunction in Atherosclerosis
Abhiram Prasad,Theresa Tupas-Habib,Theresa Tupas-Habib,William H. Schenke,Rita Mincemoyer,Julio A. Panza,Myron A. Waclawin,Samer Ellahham,Samer Ellahham,Arshed A. Quyyumi +9 more
TL;DR: The results of the present study indicate that inhibition of the AT(1) receptor in patients with atherosclerosis reverses endothelial dysfunction by improving NO availability and therefore may have long-term therapeutic benefits.