Neurohormonal activation in congestive heart failure and the role of vasopressin

Abstract

Vasoactive neurohormonal systems (eg, sympathetic nervous system [SNS], renin-angiotensin-aldosterone system, and arginine vasopressin [AVP]) are defense mechanisms designed to preserve arterial volume and circulatory homeostasis during periods of low cardiac output. Neurohormonal systems, which are normally stimulated under conditions of acute volume depletion, are activated by the low cardiac output and arterial pressure. However, sustained and chronic activation of these systems, as occurs in congestive heart failure (CHF), can cause progressive ventricular remodeling and worsening heart failure. Vasoconstriction, water retention, and increased blood volume are results of the activation of the SNS, the renin-angiotensin pathway, and AVP secretion. These effects can accelerate progression of CHF, contributing to increased morbidity and mortality. AVP regulates vascular tone and free-water reabsorption, respectively, through the vasopressin V(1a) and V(2) receptor subtypes and therefore is a potential neurohormonal target in the treatment of CHF.