Congestive heart failure (CHF) is a pathophysiological condition associated with increased plasma levels of
atrial natriuretic factor (
ANF), a
peptide hormone of cardiac origin that participates in the homeostatic control of intravascular volume and vascular tone. Atrial myocytes serve as the principal source of
ANF under physiological conditions, although recent studies have demonstrated that ventricular myocardium may also synthesize
ANF in models of CHF associated with ventricular
hypertrophy. The current study was designed to investigate the roles of atrial and ventricular myocardium to synthesize, store, and release
ANF during the evolution of
tachycardia-induced CHF in the dog. The present study demonstrates a persistent elevation of plasma
ANF during the evolution of CHF. In acute CHF (3 h), plasma
ANF increased independent of cardiac
ANF synthesis. In chronic CHF (15 and 30 days), plasma
ANF is maintained by an increase in atrial synthesis and release of the
peptide, without recruitment of ventricular
ANF synthesis. The present study demonstrates that in acute CHF the increase in plasma
ANF is regulated by release of stored
peptide, and in chronic CHF the persistent elevation of plasma
ANF is maintained by an increase in atrial synthesis of
ANF.