Author(s): Fabian Müller | Rainer H Böger | Sudha Seshadri | Renke Maas
Journal: European Neurological Journal
ISSN 2041-8000
Volume: 2;
Issue: 2;
Start page: 17;
Date: 2010;
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Keywords: Asymmetric dimethylarginine | ADMA | Carotid artery | Intima-media thickness | Atherosclerosis | Nitric oxide synthase
ABSTRACT
This review gives an overview of currently available data from clinical studies relating the endogenous nitric oxide (NO) synthase inhibitor asymmetrical dimethylarginine (ADMA) to cerebrovascular disease. In the majority of studies, ADMA plasma concentration correlates positively with the intima media thickness of the carotid artery. Moreover, elevation of plasma ADMA predicts prevalent cerebrovascular disease, progression of atherosclerosis, and adverse clinical outcome. Data from in vitro experiments and infusion studies in mice and men suggest that inhibition of NO synthesis by ADMA is a plausible pathomechanism behind these clinical findings. However, ADMA plasma concentrations associated with discernible differences in atherosclerotic burden in population-based studies are substantially lower than ADMA concentrations required to elicit functional effects in vitro. A further investigation of the metabolism and distribution of ADMA in vivo may help to resolve these issues.
Journal: European Neurological Journal
ISSN 2041-8000
Volume: 2;
Issue: 2;
Start page: 17;
Date: 2010;
VIEW PDF
DOWNLOAD PDF Original pageKeywords: Asymmetric dimethylarginine | ADMA | Carotid artery | Intima-media thickness | Atherosclerosis | Nitric oxide synthase
ABSTRACT
This review gives an overview of currently available data from clinical studies relating the endogenous nitric oxide (NO) synthase inhibitor asymmetrical dimethylarginine (ADMA) to cerebrovascular disease. In the majority of studies, ADMA plasma concentration correlates positively with the intima media thickness of the carotid artery. Moreover, elevation of plasma ADMA predicts prevalent cerebrovascular disease, progression of atherosclerosis, and adverse clinical outcome. Data from in vitro experiments and infusion studies in mice and men suggest that inhibition of NO synthesis by ADMA is a plausible pathomechanism behind these clinical findings. However, ADMA plasma concentrations associated with discernible differences in atherosclerotic burden in population-based studies are substantially lower than ADMA concentrations required to elicit functional effects in vitro. A further investigation of the metabolism and distribution of ADMA in vivo may help to resolve these issues.
