Ascites is the most common complication of cirrhosis. It is associated with profound changes in the splanchnic and systemic circulation and with renal abnormalities. The development of ascites is related to the existence of severe sinusoidal portal hypertension that causes marked splanchnic arterial vasodilation and a forward increase in the splanchnic production of lymph. Splanchnic arterial vasodilation also produces arterial vascular underfilling, arterial hypotension, compensatory activation of the RAAS, SNS, and AVP, and a continuous sodium and water retention, leading to ascites formation. Now, therefore, the splanchnic arterial circulation, rather than the venous portal system, is believed to be involved in the pathogenesis of ascites formation.