Asymmetric Dimethylarginine (ADMA) in cardiovascular and renal disease

• ADMA is formed when intracellular arginine residues are methylated by methyltransferase enzymes.
• ADMA competes with NOS and compromises NO synthesis.
• The literature suggests that high ADMA may have a role in cardiovascular/renal diseases.
• Clarifying this issue is essential for improving the management of these diseases.

BackgroundAsymmetric Dimethylarginine (ADMA) is a modified amino acid formed when intracellular arginine is methylated by methyltransferases that are widely distributed throughout the body. Nitric oxide (NO) is produced from l-arginine in a reaction catalyzed by three distinct isoforms of NO synthase (NOS). NO has emerged as a mediator involved in maintenance of vascular tonus, blood pressure regulation, inhibition of platelet aggregation, leukocyte and endothelial cell interaction and vascular permeability. ADMA is an important inhibitor that competes with NOS and compromises NO synthesis.ObjectiveThis review aims to compile articles involving renal and cardiovascular diseases in which plasma ADMA was assessed in order to clarify its role in these diseases.ConclusionAlthough current knowledge suggests that ADMA has a role in the onset of cardiovascular and renal diseases, its actions are poorly understood. Clarifying its biochemical mechanisms is essential for improving disease management and promoting better quality of life for these patients.