Figure 3.

Mechanism of action for vaptans in the treatment of hypervolemic hyponatremia. In the setting of decompensated cirrhosis, the reduction of the effective arterial blood volume results in the increased release of AVP. AVP binds to the V2 AVP receptor located on the basolateral membrane of distal collecting duct cells within the kidneys. This process activates the binding of aquaporin water channels to collecting duct cell membranes and causes increased reabsorption of water. With excessive water retention, the urine becomes solute‐concentrated, and the serum becomes dilute; this leads to hyponatremia. However, if a patient receives a vaptan drug, the vaptan prevents the binding of AVP to the V2 AVP receptor and thus inhibits water reabsorption. In turn, this results in abundant solute‐diluted urine output and maintains serum sodium homeostasis.