© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Water and sodium regulation in chronic heart failure: the role of natriuretic peptides and vasopressin
aDepartment of Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse Street, London SW3 6LY, UK
bDepartment of Cardiology, Franz-Volhard-Klinik (Charité, Campus Berlin-Buch) at Max Delbrück Centrum for Molecular Medicine, Berlin, Germany
* Corresponding author. Tel.: +44-207-351-8127; fax: +44-207-351-8733 p.kalra@ic.ac.uk
Received 15 November 2000; accepted 26 March 2001
KEYWORDS Heart failure; Natriuretic peptide; Vasoconstriction/dilation; Antihypertensive/diuretic agents
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1 Introduction |
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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
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2 Mechanisms involved in sodium and water homeostasis in chronic heart failure (Fig. 1) |
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3 The natriuretic peptide family |
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3.1 Structure
3.2 Receptors and metabolism (Fig. 2a)
3.3 Natriuretic peptide release
3.4 Plasma and urine levels of natriuretic peptides
3.5 Biological effects of the natriuretic peptides
3.5.1 Natriuresis and diuresis
3.5.2 The role of natriuretic peptides in CHF — data from experimental models and small studies of human CHF
3.5.2.1 ANP
3.5.2.2 BNP
3.5.2.3 CNP
3.5.3 Other biological effects of the natriuretic peptides
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4 Vasopressin |
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4.1 Vasopressin receptors and water channels (Fig. 2b)
4.1.1 The role of vasopressin in CHF — data from experimental models and small studies of human CHF
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5 Clinical trials involving natriuretic peptides and vasopressin antagonism in CHF |
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5.1 Natriuretic peptides
5.1.1 Therapy guided by plasma natriuretic peptide levels
5.1.2 Vasopeptidase inhibition
5.1.3 Intravenous recombinant human BNP
5.2 Vasopressin receptor antagonists
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6 Conclusions |
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