Hyponatremia in Heart Failure: The Role of Arginine Vasopressin and Its Antagonism

Authors


Mitchell H. Rosner, MD, Division of Nephrology, Department of Medicine, University of Virginia Health System, Box 800133, Charlottesville, VA 22908
E-mail: mhr9r@virginia.edu

Abstract

Congest Heart Fail. 2010;16(4)(suppl 1):S7–S14. ©2010 Wiley Periodicals, Inc.

Heart failure (HF) is associated with substantial cost, morbidity, and mortality. One of the common complications associated with HF, as well as with its treatment, is the development of hyponatremia. Hyponatremia is due to the nonosmotic release of arginine vasopressin (AVP) along with neurohormonal activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. Hyponatremia in patients with HF is associated with poor outcomes and can limit the use of diuretic therapy. Given that AVP is the primary stimulus for the development of hyponatremia in these patients, therapies that target AVP action would seem a logical choice in the therapeutic regimen for HF. Drugs that antagonize the action of AVP at the vasopressin V2 receptor, which is primarily responsible for water resorption in the kidney, are now available and have been studied in patients with HF. These drugs (termed vaptans) have been associated with improvements in serum sodium concentration, urine output, body weight, and mental functioning but have shown no long-term mortality benefit in patients with HF. The role of vaptans in the HF armament will require further studies that center on the proper timing and indications for their use as well as their cost-efficacy.

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