Dimethylarginines occur with transmethylation of arginine by the enzyme protein methyl transferase (PRMT). Then, methylated arginine undergoes proteolysis and converts to asymetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) which is not active biologically. Liver and kidney have an important role in the production and excretion of ADMA. Dimethylarginine dimethylaminohydrolase (DDAH) is the main enzyme, responsible for the metabolism of ADMA. Liver is the main organ which the enzyme substantially exists. But the enzyme may also be found in kidney, brain, adrenal glands, pancreas and testis. ADMA is eliminated especially by DDAH-1 in the liver and also excreted by bile and urine. Plasma ADMA concentration increases in patients with hepatic dysfunction, end-stage renal disease, endothelial dysfunction and increased risk of atherosclerosis. Also increased ADMA levels have been shown to lead to the development of hepatorenal syndrome (HRS). It has been reported that accumulation of ADMA increases the liver damage in patients with cirrhosis. ADMA is the direct inhibitor of nitric oxide synthase (NOS), the enzyme responsible for the synthesis of nitric oxide (NO). NO is involved in maintaining vascular tonus. The reduction in NO levels caused by increased levels of ADMA, increases liver damage in cirrhosis via increasing intrahepatic vascular resistance. In this review; relationship between liver and ADMA, ADMA and its effect on NO formation and action mechanism, effect of increased ADMA levels in liver damage on organs and systems will be discussed.