The atrial peptide system in cardiac disease.

Abstract

Atrial natriuretic factor (ANF) is a peptide hormone of cardiac origin, released in response to atrial distention, that increases sodium excretion, inhibits the renin-angiotensin-aldosterone (RAA) system, and decreases arterial pressure. Congestive heart failure (CHF) is a clinical syndrome that is characterized by chronic atrial distention, sodium retention with edema, and activation of the RAA system. The role of ANF in the pathophysiology of CHF remains to be defined. Circulating ANF is greatly increased in congestive heart failure. The mechanism of this elevation of ANF is explained by increased synthesis and release of ANF from the atria with atrial depletion of ANF in response to chronic atrial overload. Recent work also suggests the presence of ANF in ventricular myocardium in heart failure in which the ventricle is recruited to synthesize and release this peptide hormone. Despite increased circulating ANF in heart failure, the kidney retains sodium and is hyporesponsive to exogenous administration of ANF. The mechanism of this hyporesponsiveness is multifactorial but may be explained in part by activation of the intrarenal RAA system as well as by a reduction in renal perfusion pressure. A therapeutic role for ANF remains unclear. To date, studies conflict, but some investigations of ANF infusions in man support a unique and selective renal vasodilator action in association with an ability to inhibit the RAA system.