Hyponatremia is independently associated with adverse outcomes in patients with congestive heart failure (CHF). The primary cause of hyponatremia in CHF is the inappropriate secretion of the antidiuretic hormone, arginine vasopressin (AVP). The binding of AVP to V2 receptors in the renal collecting duct promotes water retention, a process that can lead to dilutional hyponatremia as well as increased ventricular preload. AVP could also exacerbate the course of CHF by interacting with V1A receptors on vascular smooth muscle cells and myocytes. Conventional treatment of hyponatremia in CHF is based largely on water restriction, which is neither effective nor well tolerated. Current research is exploring V2- and dual V1A/V2-receptor antagonism for the treatment of hyponatremia, as well as for the congestion and edema associated with CHF, since AVP-receptor antagonists may offer benefits in comparison to conventional loop diuretics. Clinical trials in patients with hyponatremia and CHF using both selective and nonselective vasopressin antagonists have demonstrated the effectiveness of these agents in correcting this common electrolyte abnormality.