In the presence of a primary disorder in myocardial contractility and/or extraordinary hemodynamic pressure on the heart, ventricular performance depends on several compensating mechanisms. In the past, studies were mostly focused on the importance of the Frank-Starling mechanism and the hypertrophy and dilation of the heart in maintaining a circulation sufficient for metabolic intake during heart failure. Recently, however, the existence of neurohormonal systems has been demonstrated (the sympathetic nervous system, the renin-angiotensin system, atrial natriuretic peptide and several locally produced vasoactive substances), which change considerably according to the severity of the heart failure. While these compensatory mechanisms support the circulation in patients with acute heart failure, in whole or in part, neurohormonal activation over an extended period of time might be harmful to patients with chronic congestive heart failure since several neurohormonal factors might be inappropriately activated. This article will review the key neurohormonal systems and their importance in heart failure on the basis of the current literature.