Neurohormonal abnormalities contribute to the pathophysiology of congestive heart failure (CHF). Successful approaches to improving the prognosis of patients with CHF are based largely on therapeutic interruption of activated neurohormonal systems. The use of antagonists and inhibitors of the renin-angiotensin-aldosterone and sympathetic nervous systems has significantly improved clinical outcomes in CHF. Excessive secretion of arginine vasopressin (AVP) has the potential for deleterious effects on various physiologic processes in CHF. Inhibition of AVP through vasopressin receptor antagonist therapy is a potentially beneficial new therapeutic approach to CHF.