Portal hypertension is defined as a rise in the pressure gradient between the portal vein and the inferior vena cava by more than 10 mmHg. The basic factors in the development of portal hypertension include increased resistance in intrahepatic circulation, increased portal blood flow, and development of the hyperdynamic syndrome. Apart from structural changes in the hepatic tissue, the major role in the pathogenesis of portal hypertension is played by endothelial dysfunction. In patients with portal hypertension, endothelial dysfunction reduced the activity of vasodilator, anti-aggregation, and anti-adhesion substances (NO/EDRF, prostacyclin, CO) and to increased production of vasoconstrictor and proliferative substances (endothelins in particular) in intrahepatic the circulation. On the other hand, vasodilator agents become predominant in splanchnic and systemic circulation. As a result, the intrahepatic vascular resistance and portal blood flow rise. It was followed by a subsequent increase in portal pressure and the development of hyperdynamic circulation. Identification of the pathophysiological mechanisms of portal hypertension has paved the way to new trends in pharmacological therapy. The aim of effective treatment of portal hypertension is the permanent reduction of the portal pressure, which markedly decreases the risk for complications, and the risk for esophageal variceal bleeding in particular. The currently most preferred agents are those with vasodilator and vasoconstrictor effects.

        Key words: portal hypertension, endothelial dysfunction, vasoactive factors, intrahepatic resistance, hyperdy- namic circulation, treatment of portal hypertension