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There are multiple receptors for vasopressin (ADH) named the V1a, V1b, and V2 receptors. The V2 receptors primarily mediate the antidiuretic response, while V1a and V1b receptors principally cause vasoconstriction and mediate adrenocorticotropin release, respectively. Some oral formulations of vasopressin receptor antogonists - tolvaptan, satavaptan, and lixivaptan — are selective for the V2 receptor, while an intravenous agent, conivaptan, blocks both the V2 and V1a receptors and is approved for the management of patients with euvolemic hyponatremia (mostly due to SIADH) and hypervolemic hyponatremia. The vasopressin receptor antagonists produce a selective water diuresis without affecting sodium and potassium excretion. The ensuing loss of free water will tend to correct the hyponatremia in patients with SIADH. Elevated levels of vasopressin may contribute to the increase in systemic vascular resistance in heart failure via stimulation of the V1a receptor, which is found on vascular smooth muscle cells, and also promote renal water retention via the V2 receptor, leading to the development of hyponatremia. At present, conivaptan is the only vasopressin receptor antagonist approved for use. In patients with heart failure, conivaptan both raises the serum sodium concentration and, via blockade of the V1a receptors, diminishes afterload, possibly improving systemic hemodynamics. V2 receptor antagonists (aquaretics) have a critical role in the management of the hyponatremia of SIADH, heart failure, ascites of hepatic failure and they may also diminish the cystogenesis in the early stages of polycystic kidney disease.