Asymmetric dimethylarginine (ADMA) determines the improvement of hepatic endothelial dysfunction by vitamin E in cirrhotic rats.

摘要: Background Hepatic endothelial dysfunction (HED), which is caused by decreased hepatic nitric oxide (NO) bioavailability and increased lipid peroxidation, contributes to portal hypertension, a characteristic of cirrhosis. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor synthase (NOS), involved in cirrhosis-related HED hypertension. Aims We evaluated the effect vitamin E treatment on hypertension cirrhotic rats. Methods The common bile duct ligation (BDL)-induced rats were treated orally either with vehicle or for 1 month immediately after BDL. Systemic haemodynamics, magnitude increase pressure induced volume expansion, HED, oxidative stress, levels ADMA, various proteins mRNAs then measured. Results In E-treated BDL rats, decrease was associated attenuation expansion. In isolated perfused rat livers, significantly inhibited (paradoxical) vasoconstriction response methoxamine acetylcholine this abolished presence NOS. Vitamin ADMA synthesizing enzyme PRMT1 expression level thiobarbituric acid-reactive substances (TBARS) liver, while increasing metabolizing DDAH2, eNOS, phosphor-eNOS, superoxide dismutase activity. Conclusions The administration suppressed stress liver circulation, therefore increases NO bioavailability, improved hypertension.