Cirrhosis of the liver is by far the most common cause of portal hypertension in the western world. Portal hypertension is a frequent clinical syndrome, defined by a pathological increase in the portal venous pressure. When the portal pressure gradient (the difference between pressures in the portal and the inferior vena cava veins: normal value below 6 mmHg) increases above 10-12 mmHg, complications of portal hypertension can occur. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in great part due to morphological changes occurring in chronic liver diseases. However, more recently a graded and reversible contraction of different elements of the porto-hepatic bed have been shown to play a role modulating intrahepatic vascular resistance which provides a rationale for the intention to reduce intrahepatic resistance and portal pressure by means of pharmacological agents. The subsequent increase in portal blood flow, as a result of the arteriolar vasodilatation of the splanchnic organs, plays a contributory role maintaining and aggravating the portal hypertensive syndrome. This splanchnic arteriolar vasodilatation is a multifactorial phenomenon, which may involve neurogenic, humoral and local mechanisms.