Water and sodium regulation in chronic heart failure: the role of natriuretic peptides and vasopressin

Extract

Time for primary review 28 days.

1 Introduction

Chronic heart failure (CHF) is a complex syndrome characterised by objective evidence of ventricular dysfunction and associated clinical symptoms [1]. Activated neurohormonal mechanisms play an important role in the maintenance of circulatory homeostasis. They can be divided into the vasoconstrictive, sodium retaining and the opposing vasodilatory, natriuretic systems. Vasoconstrictive and sodium retentive actions are provided by the renin–angiotensin–aldosterone system, the sympathetic nervous system, vasopressin, thromboxane and endothelin [2–5]. Initially, in patients with heart failure, these act as important compensatory mechanisms maintaining blood pressure and adequate tissue perfusion. However, prolonged activation of these systems has deleterious effects on haemodynamics and directly on the heart itself. Enhanced vasoconstriction and fluid retention result in adverse loading conditions in the failing ventricle, whilst high levels of angiotensin II directly induce cardiac myocyte necrosis and adversely alter the myocardial matrix structure [6–9]. Angiotensin II also potentiates sympathetic drive by direct stimulation and by impairing its control by the baroreceptors [10].