The Molecules: Abnormal Vasculatures in the Splanchnic and Systemic Circulation in Portal Hypertension

Portal hypertension, defined as an increase in pressure within the portal vein, is a detrimental complication in liver diseases. The increased intrahepatic resistance as a consequence of cirrhosis is the primary cause of portal hypertension (Figure 1). Once it is developed, portal hypertension influences extrahepatic vascular beds in the splanchnic and systemic circulation. Two major consequences of portal hypertension in this regard are excessive arterial vasodilation/hypocontractility and the formation of portosystemic collateral vessels. Both excessive arterial vasodilation and portosystemic collateral vessel formation help to increase the blood flow through the portal vein and worsen portal hypertension. This facilitates the development of the abnormal hemodynamic condition, called the hyperdynamic circulatory syndrome, and ultimately leads to variceal bleeding and ascites (Bosch 2000; Bosch 2007; Groszmann 1993; Iwakiri 2011; Iwakiri & Groszmann 2006).