This review summarizes recent progress in the knowledge of catecholamines in cirrhosis. Compensated patients have normal plasma concentration of noradrenaline. Highly elevated plasma noradrenaline concentration in decompensated patients indicates that the sympathetic nervous system is enhanced in this condition. This may especially apply to the sympathetic tone in the kidney, as evaluated by regional measurements of noradrenaline overflow. Hepatic elimination of catecholamines is only slightly reduced. Activation of the sympathetic nervous system seems to play an important role in the avid sodium-water retention and decreased kidney perfusion observed in decompensated cirrhosis. Volume- en baro-receptors are likely to elicit this overactivity. The decreased systemic arterial blood pressure may be a primary event which is in part counteracted by enhanced sympathetic nervous activity and activated renin-angiotensin system. The role of a non-volume-dependent hepatic baro-receptor, false neurotransmitters, postsynaptic receptors, and autonomous neuropathy are yet unknown issues of further research.