Impaired cardiac function is of course the primary problem in heart failure, but it is also the stimulus to activation of several integrated neuroendocrine systems. Activation of these neuroendocrine systems at first seems to have important beneficial effects for the failing circulation-maintaining cardiac output, blood pressure, blood flow to essential organs, and the glomerular filtration rate. Prolonged or extreme neuroendocrine activation, however, may prove deleterious.

The advent of effective diuretics had a tremendous impact on the management of patients with heart failure. Then, in the absence of a cure for the primary problem, thoughts returned to agents that either increased the force of myocardial contraction (inotropic agents) or reduced the load on the failing heart (vasodilator agents). Both modes of treatment have proved effective in improving haemodynamic function in the short term. Neither therapeutic intervention has yet been established as having beneficial effects for long term treatment of heart failure. A fourth group of agents was added to the treatment of heart failure in the 1980s. The angiotensin converting enzyme(ACE) inhibitors have showed not only their ability to improve symptoms and exercise perfor-mance, but also to reduce mortality and possibly slow the rate of decline in ventricular function. In the 1990s their use is certainly going to increase. These agents are more than just another group of vasodilator agents. Their effects on neuroendocrine activity seem to be integral to their success. A review of the interaction between neuroendocrine variables and vasodilator therapy is timely.