ADMA and hyperhomocysteinemia

Sanjana Dayal; Steven R Lentz

doi:10.1177/1358836X0501000105

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Journal article

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ADMA and hyperhomocysteinemia

Sanjana Dayal and Steven R Lentz

Vascular medicine (London, England), Vol.10 Suppl 1(1_suppl), pp.S27-S33

07/2005

DOI: 10.1177/1358836X0501000105

PMID: 16444866

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Abstract

Hyperhomocysteinemia is a risk factor for cardiovascular disease and stroke. Like many other cardiovascular risk factors, hyperhomocysteinemia produces endothelial dysfunction due to impaired bioavailability of endothelium-derived nitric oxide (NO). The molecular mechanisms responsible for decreased NO bioavailability in hyperhomocysteinemia are incompletely understood, but emerging evidence suggests that asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, may be a key mediator. Homocysteine is produced during the synthesis of ADMA and can alter ADMA metabolism by inhibiting dimethylarginine dimethylaminohydrolase (DDAH). Several animal and clinical studies have demonstrated a strong association between plasma total homocysteine, plasma ADMA, and endothelial dysfunction. These observations suggest a model in which elevation of ADMA may be a unifying mechanism for endothelial dysfunction during hyperhomocysteinemia. The recent development of transgenic mice with altered ADMA metabolism should provide further mechanistic insights into the role of ADMA in hyperhomocysteinemia.

Enzyme Inhibitors - blood

Humans

Hyperhomocysteinemia - metabolism

Endothelium, Vascular - drug effects

Homocysteine - metabolism

Endothelium, Vascular - enzymology

Arginine - analogs & derivatives

Vasodilation

Homocysteine - pharmacology

Superoxides - metabolism

Cardiovascular Diseases - blood

Nitric Oxide Synthase Type III - metabolism

Disease Models, Animal

Amidohydrolases - metabolism

Cardiovascular Diseases - etiology

Hyperhomocysteinemia - blood

Cardiovascular Diseases - metabolism

Enzyme Inhibitors - metabolism

Risk Factors

Enzyme Inhibitors - pharmacology

Homocysteine - blood

Amidohydrolases - antagonists & inhibitors

Nitric Oxide Synthase Type III - antagonists & inhibitors

Animals

Arginine - blood

Arginine - pharmacology

Nitric Oxide - metabolism

Hyperhomocysteinemia - complications

Arginine - metabolism

Details

Title: Subtitle: ADMA and hyperhomocysteinemia
Creators: Sanjana Dayal - Department of Internal Medicine, University of Iowa, Iowa City 52242, USA
Steven R Lentz
Resource Type: Journal article
Publication Details: Vascular medicine (London, England), Vol.10 Suppl 1(1_suppl), pp.S27-S33
Publisher: England
DOI: 10.1177/1358836X0501000105
PMID: 16444866
ISSN: 1358-863X
eISSN: 1477-0377
Grant note: HL63943 / NHLBI NIH HHS NS24621 / NINDS NIH HHS
Language: English
Date published: 07/2005
Academic Unit: Hematology, Oncology, and Blood & Marrow Transplantation; Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
Record Identifier: 9984065389402771

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