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Asymmetric Dimethylarginine (ADMA)

Asymmetric dimethylarginine (ADMA) measurement is used in assessing the likelihood of future coronary events in patients with coronary heart disease, type II diabetes mellitus, hypercholesterolemia, or kidney disease.

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Dimethylarginines, asymmetric (ADMA) and symmetric (SDMA), are the methyl derivates of L-arginine, present in human blood at micromolar levels. They are the result of the degradation of methylated proteins during hydrolytic protein turnover.

ADMA inhibits nitric oxide (NO) synthesis via competitive inhibition of nitric oxide synthase (NOS). SDMA does not interfere with NOS activity directly but may still have an inhibitory effect on NO synthesis by suppressing cellular uptake of its precursor, L-arginine, and by inhibiting renal tubular absorption of L-arginine.

NO has multiple targets in humans, including cardiovascular, nervous, and inflammation/immunology systems. NO is an important vasodilator that regulates systemic blood pressure. NO inhibits superoxide generation, the interaction of circulating blood elements with the vessel wall, as well as platelets adhesion and aggregation, smooth muscle cell proliferation, and the accumulation of lipids within the vessel wall. Its deficiency results in endothelial dysfunction and atherosclerotic vascular complications. NO may also have a role in the regulation of apoptosis, angiogenesis, cell cycle, invasion, and metastasis of malignant cells.

Increased ADMA plasma levels are linked to endothelial dysfunction, vasoconstriction, the elevation of blood pressure, and the aggravation of experimental atherosclerosis. Elevated plasma ADMA concentrations have been noted in numerous clinical conditions associated with NO-dependent endothelial dysfunction, e.g., hypercholesterolemia, hypertension, myocardial infarction, chronic renal failure, chronic heart failure, diabetes mellitus, homocysteinemia, and peripheral arterial disease.

The strongest association between ADMA and all-cause mortality has been observed in critically ill patients from intensive care units (ICU), but the statistically significant relations with all-cause mortality have also been noted in the general population, in patients with renal diseases, peripheral arterial disease and in those with prevalent cardiovascular diseases (CVD).

ADMA and SDMA have different clearance pathways. SDMA and partially ADMA are excreted unchanged by the kidney and some amount of ADMA and less of SDMA is a subject of biliary excretion. However, the major metabolic pathway of ADMA involves its degradation by dimethylarginine dimethyloaminohydrolase (DDAH) into dimethylamine (DMA) and L-citrulline (CIT). The metabolites of ADMA are excreted in the urine.

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