Patients with cirrhosis and portal hypertension exhibit characteristic haemodynamic changes with a hyperkinetic systemic circulation, an abnormal distribution of the blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased, but the central and arterial blood volume and systemic vascular resistance are decreased. A systemic and splanchnic vasodilatation is of pathogenic importance to the low systemic vascular resistance and abnormal volume distribution. These are important elements in the development of the low arterial blood pressure and hyperkinetic circulation in cirrhosis. Various vasodilators such as nitric oxide, calcitonin gene-related peptide, and adrenomedullin are among potential candidates in the vasodilatation in cirrhosis. Besides reflex induced enhanced sympathetic nervous activity, activation of the renin-angiotensin-aldosterone system, and elevated circulation vasopressin, endothelin-1 may also be implicated in the haemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the haemodynamic and neurohumoral abnormalities in cirrhosis are part of a general circulatory dysfunction, influencing the course of the disease with reduction of kidney function and sodium-water retention as the outcome.