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Cardiac atrial natriuretic factor during evolution of congestive heart failure
M A Perrella1, T R Schwab, B O'Murchu
1Department of Cardiovascular Disease, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
Insights
Congestive heart failure (CHF) elevates atrial natriuretic factor (ANF) levels. In acute CHF, ANF release increases from stores, while chronic CHF relies on enhanced atrial ANF synthesis.
Area of Science:
- Cardiology
- Endocrinology
- Physiology
Background:
- Congestive heart failure (CHF) is linked to elevated atrial natriuretic factor (ANF) levels.
- ANF, a peptide hormone, regulates intravascular volume and vascular tone.
- While atria are the primary ANF source, ventricles may synthesize it in CHF with hypertrophy.
Purpose of the Study:
- To investigate atrial and ventricular myocardium roles in ANF synthesis, storage, and release during tachycardia-induced CHF in dogs.
- To elucidate the mechanisms behind elevated plasma ANF in evolving CHF.
Main Methods:
- Induction of CHF via tachycardia in canine models.
- Measurement of plasma ANF levels at acute (3 hours) and chronic (15 and 30 days) stages.
- Assessment of cardiac ANF synthesis and release dynamics.
Main Results:
- Plasma ANF remained persistently elevated throughout CHF evolution.
- In acute CHF, increased plasma ANF was independent of cardiac synthesis, suggesting release from stores.
- Chronic CHF (15-30 days) showed sustained high plasma ANF due to increased atrial synthesis and release, without ventricular recruitment.
Conclusions:
- Acute CHF elevates plasma ANF primarily through the release of stored peptide.
- Chronic CHF maintains elevated plasma ANF levels via enhanced atrial ANF synthesis and release.
- Ventricular ANF synthesis is not recruited to compensate for chronic CHF in this model.
Abstract:
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.