This paper reviews the evidence that congestive heart failure is characterized by an increase in sympathetic nerve activity and that this may begin in an early symptomatic phase and progress with the severity of the disease. The sympathetic activation initially plays a compensatory role but eventually is outweighted by adverse consequences at both cardiac and vascular levels which may aggravate the clinical status and negatively affect prognosis. This is likely to depend on the fact that the sympathetic activation becomes excessive due to reduction in sensitivity of baroreflexes and cardiopulmonary reflexes restraining sympathetic tone (functional reflex denervarion) and positive interactions between the sympathetic and the renin-angiotensin system. Therapeutic interventions may reduce the marked sympathetic activation which occurs in heart failure, and in some instances (particularly with digitalis compounds) may also improve the impaired sensitivity of reflex cardiovascular control.