Asymmetric dimethylarginine as a mediator of vascular dysfunction in cirrhosis

Figure 1 Different asymmetric dimethylarginine metabolism in liver and splanchnic circulation in portal hypertension and cirrhosis. A simplified scheme of different asymmetric dimethylarginine (ADMA) metabolism showing that dimethylarginine dimethylamohydrolase (DDAH) activity is reduced in the cirrhotic liver leading to accumulation of ADMA and decreased nitric oxide (NO) synthesis producing and increase of hepatic vascular tone. On the other hand, in splanchnic circulation portal hypertension and cirrhosis induce and increased expression and function of DDAHs, reducing ADMA levels and increasing NO bioavailability that could cause splanchnic vasodilation.