We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension (n = 9) compared with normal controls (n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric...

BACKGROUND Recent studies have revealed a higher rate of cardiovascular complications in primary aldosteronism (PA) compared to patients with essential hypertension (EH). Asymmetric dimethylarginine (ADMA) is a marker of endothelial dysfunction that could contribute to increased cardiovascular risk in patients with PA. OBJECTIVES The aim of this study was to compare the levels of ADMA among p...

Cardiovascular disease is the leading cause of mortality in patients with chronic kidney disease. Endothelial cell injury and apoptosis may promote atherosclerosis and cardiovascular disease. The present study investigated the potential mechanisms of asymmetric dimethylarginine (ADMA)‑induced apoptosis in human umbilical vein endothelial cells (HUVECs). It was demonstrated that ADMA decreased B...

Aim: Although underlying mechanisms of coronary artery ectasia (CAE) are clearly unknown, endothelial dysfunction may be responsible for the coronary ectasia. Asymmetric dimethylarginine (ADMA) is the principal endogenous inhibitor of nitric oxide synthase and elevated levels of ADMA is considered to be a marker of endothelial dysfunction and increased risk of cardiovascular disease. Accordingl...

The enzyme dimethylarginine dimethylaminohydrolase (DDAH) metabolizes asymmetrically methylated arginine (namely L-N monomethylarginine [L-NMMA] and asymmetrical dimethylarginine [ADMA]) residues to citrulline and methylamine.1 Considerable interest has been focused on the biology of DDAH after the discovery that asymmetrically methylated arginines (in particular ADMA) are competitive inhibitor...

Asymmetric Dimethylarginine and Cerebrovascular Disorders in Humans To the Editor: We read with great interest the recent article by Dr Kielstein and colleagues1 dealing with the cerebrovascular effects of the endogenous nitric oxide (NO) synthase inhibitor, asymmetric dimethylarginine (ADMA), in humans. The results of their study demonstrated that systemic infusion of ADMA increased arterial s...

We explored the role of asymmetrical dimethylarginine (ADMA) as a cause of endothelial dysfunction induced by systemic inflammation. In vitro data suggest that ADMA bioavailability is regulated by proinflammatory stimuli, but it is unclear whether ADMA is a link between inflammation and endothelial dysfunction in humans. In study 1 we recruited 351 patients with coronary artery disease (CAD) an...

Asymmetrical Dimethylarginine, Oxidative Stress, and Atherosclerosis To the Editor: Antoniades et al1 reported on the role of asymmetrical dimethylarginine (ADMA) in inflammation-induced endothelial dysfunction in healthy subjects and in patients with coronary artery disease or rheumatoid arthritis. In patients with chronic inflammatory rheumatic diseases, serum nitrite concentrations were lowe...

BACKGROUND We previously showed that increased asymmetric dimethylarginine (ADMA) biliary excretion occurs during hepatic ischemia/reperfusion (I/R), prompting us to study the effects of the farnesoid X receptor (FXR) agonist obeticholic acid (OCA) on bile, serum and tissue levels of ADMA after I/R. MATERIAL AND METHODS Male Wistar rats were orally administered 10mg/kg/day of OCA or vehicle f...