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The atrial peptide system in cardiac disease
1Department of Medicine, Mayo Medical School, Rochester, Minnesota 55905.
Insights
Atrial natriuretic factor (ANF) levels increase in congestive heart failure (CHF), yet the kidneys remain unresponsive. This study explores the complex role of ANF in CHF pathophysiology and its potential therapeutic applications.
Area of Science:
- Cardiology
- Endocrinology
- Nephrology
Background:
- Atrial natriuretic factor (ANF) is a cardiac hormone regulating sodium balance and blood pressure.
- Congestive heart failure (CHF) involves atrial distention, sodium retention, and renin-angiotensin-aldosterone (RAA) system activation.
- The precise role of ANF in CHF pathophysiology is not fully understood.
Purpose of the Study:
- To investigate the elevated levels and role of ANF in congestive heart failure.
- To explore the mechanisms behind renal hyporesponsiveness to ANF in CHF.
- To evaluate the potential therapeutic applications of ANF in heart failure.
Main Methods:
- Analysis of circulating ANF levels in CHF patients.
- Investigation of ANF synthesis and release from cardiac chambers.
- Assessment of renal response to exogenous ANF administration in CHF models.
Main Results:
- Circulating ANF levels are significantly elevated in CHF.
- Increased ANF synthesis and release occur from both atria and ventricles in heart failure.
- The kidneys exhibit hyporesponsiveness to ANF, retaining sodium despite elevated levels.
- Potential mechanisms for hyporesponsiveness include intrarenal RAA activation and reduced renal perfusion pressure.
Conclusions:
- Despite elevated ANF in CHF, renal sodium excretion is impaired due to hyporesponsiveness.
- Therapeutic use of ANF in CHF is unclear, with conflicting study results.
- ANF may possess selective renal vasodilator and RAA inhibitory actions.
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.