Arginine vasopressin in heart failure.

Pathogenesis of AVP Release In several animal models of low-output and high-output cardiac failure and in congestive heart failure in humans, it has been demonstrated that plasma AVP, renin activity, aldosterone and norepinephrine are significantly increased.7 Renal excretion of sodium and water is predominantly regulated by the integrity of the arterial circulation, which is determined by cardiac output and peripheral vascular resistance. Several baroreceptors on the high pressure side of the circulation can sense arterial underfilling, and they are found in the left atrium, carotid sinus, aortic arch and renal afferent arterioles. Reduction in baroreceptor sensitivity occurs because of a decrease in systemic arterial pressure, stroke volume, renal perfusion or mpaired water excretion is primarily involved in water retention in congestive heart failure. In 1981, Schrier’s group initially demonstrated increased release of arginine vasopressin (AVP) despite hypo-osmolality in congestive heart failure.1 Several recent studies have clarified that dilutional hyponatremia predicts the long-term outcome of heart failure, and that this pathological state is profoundly linked to nonosmotic release of AVP.2,3 The timely study by Imamura et al4 in the present issue of the Journal showed that higher plasma AVP levels were significantly linked to reduced survival in patients with congestive heart failure, in association with hyponatremia. In 2010, tolvaptan, a non-peptide AVP V2 receptor antagonist, enables us to treat water retention and hyponatremia in patients with heart failure.5,6 Since then, the pathological role of AVP has become an issue of interest to cardiologists. I