Arginine vasopressin (AVP) functions in the regulation of plasma osmolarity and blood pressure. In
heart failure, AVP worsens
heart failure by causing vasoconstriction of arteries and veins, potentially contributing to remodeling of the left ventricle and causing fluid retention and worsening of
hyponatremia. Two V(2)-receptor antagonists,
tolvaptan and
lixivaptan, and one combined V(1a)- and V(2)-receptor antagonist,
conivaptan, have shown promise for use in patients with
heart failure. All three agents have been shown to increase free water excretion and increase serum
sodium levels while maintaining serum
potassium levels. They have not been shown to decrease renal function or the glomerular filtration rate and are well tolerated, with thirst being the major adverse effect during clinical trials. Because of their effects on
sodium,
vasopressin antagonists need to be carefully monitored to ensure that serum
sodium levels do not increase too quickly and put the patient at risk for overcorrection or osmotic
demyelination syndrome. In addition, patients need to be monitored for signs of
dehydration secondary to increased urine excretion. To date, studies have not consistently shown improvements in patient symptoms or
weight reduction. However, early data suggest that at least one agent,
tolvaptan, does not alter mortality.
CONCLUSION: