Vascular endothelium is responsible for the synthesis of vasodilating and vasoconstriction factors. Its damage means disorder or loss, among others ability to synthesize and release vasodilators, including nitric oxide (NO). In liver cirrhosis, there is a loss of fenestration, increased vasoconstriction and reduced bioavailability of NO (endothelial damage indicator), which can lead to increased intrahepatic resistance and the development of portal hypertension.

Asymmetric dimethylarginine (ADMA) – an inhibitor of endothelial nitric oxide synthase (eNOS) is responsible for reduced NO production. Mediators of the inflammatory reaction: tumor necrosis factor-α, κB nuclear transcription factor, Toll-like receptors, angiotensin II, endothelin-1, protease-activated receptors or adiponectin inhibit eNOS by increasing ADMA concentration. Overproduction of ROS contributes to the weakening of eNOS activity and NO uptake.

Therapy with antioxidants, statins, nuclear receptors, β-blockers, ammonia lowering agents and angiotensin receptor antagonists allows the restoration of normal endothelial function and prevents the development of portal hypertension in cirrhosis.

Keywords: vascular endothelium, liver cirrhosis, therapy strategies.