The accumulation of ascites in cirrhosis had been classically attributed to the transudation of fluid from the splanchnic vascular bed to the peritoneal cavity due to the presence of portal hypertension. This transudation of fluid would induce hypovolemia responsible for the renal abnormalities frequently observed in these patients. Recent studies, however, indicate that the pathophysiology of ascites in cirrhosis is far more complex. Cirrhotic patients with ascites usually have profound disturbances in systemic hemodynamics and renal function and an activation of the endogenous vasoactive systems that contribute to the formation of ascites. In the present article the pathogenesis of these disturbances and their possible contribution to the formation of ascites are discussed.