Atrial natriuretic peptide is a peptide hormone of cardiac origin, whi
ch is released in response to atrial distension and serves to maintain
sodium homeostasis and inhibit activation of the renin-angiotensin-al
dosterone system. Congestive heart failure is a clinical syndrome char
acterized by increased cardiac volume and pressure overload with an in
ability to excrete a sodium load, which is associated with increased a
ctivity of systemic neurohumoral and local autocrine and paracrine mec
hanisms. Circulating atrial natriuretic peptide is greatly increased i
n congestive heart failure as a result of increased synthesis and rele
ase of this hormone. Atrial natriuretic peptide has emerged as an impo
rtant diagnostic and prognostic serum marker in congestive heart failu
re. In early heart failure, it may play a key role in preserving the c
ompensated state of asymptomatic left ventricular dysfunction. Despite
increased circulating atrial natriuretic peptide in heart failure, th
e kidney retains sodium and is hyporesponsive to exogenous and endogen
ous atrial natriuretic peptide. The mechanism for the attenuated renal
response is multifactorial and includes renal hypoperfusion, activati
on of the renin-angiotensin-aldosterone and sympathetic nervous system
s. Therapeutic strategies to potentiate the biologic actions of atrial
natriuretic peptide may prolong the asymptomatic phase and delay prog
ression to overt congestive heart failure.