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Updated: Dec 30, 2025
Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
Heart is the Target Organ of Endogenous Cardiac Natriuretic Peptides
Takayoshi Tsutamoto1, Hiroshi Sakai1, Takashi Yamamoto1
1Department of Cardiovascular Medicine, Shiga University of Medical Science.
Insights
The failing heart produces cyclic guanosine monophosphate (cGMP), indicating it is the target organ for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in heart failure with reduced ejection fraction (HFrEF).
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are key hormones in cardiovascular regulation.
- Their role as endogenous effectors in heart failure with reduced ejection fraction (HFrEF) remains incompletely understood.
- Cyclic guanosine monophosphate (cGMP) serves as a crucial second messenger for ANP and BNP signaling.
Purpose of the Study:
- To investigate whether the heart acts as a target organ for endogenous ANP and BNP in HFrEF patients.
- To measure cardiac production of cGMP, a downstream marker of natriuretic peptide activity.
Main Methods:
- Plasma cGMP levels were measured in the aortic root (AO) and coronary sinus (CS) of 237 HFrEF patients.
- Patients were stratified into mild (NYHA II) and severe (NYHA III-IV) heart failure groups.
- Correlations between natriuretic peptides, cGMP, hemodynamics, and therapy were analyzed.
Main Results:
- Significantly higher cGMP levels were found in the CS compared to the AO in mild HF patients (NYHA II).
- No significant difference in cGMP was observed between CS and AO in severe HF patients (NYHA III-IV).
- In mild HF, cardiac production of cGMP correlated with ANP and BNP levels, and AO ANP+BNP predicted (CS-AO) cGMP.
Conclusions:
- The failing heart actively produces cGMP, confirming it as a target organ for endogenous ANP and BNP in HFrEF.
- cGMP production may be attenuated in severe HFrEF, potentially due to receptor downregulation or increased degradation.
- These findings highlight differential natriuretic peptide signaling in varying stages of heart failure.
Abstract:
This study aimed to evaluate whether the heart is the target organ of endogenous atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in patients with heart failure (HF) with reduced ejection fraction (HFrEF).We measured the plasma levels of cyclic guanosine monophosphate (cGMP), which is a second messenger of ANP and BNP, in the aortic root (AO) and coronary sinus (CS) in 237 patients with HFrEF. Plasma levels of cGMP were significantly higher in the CS than those in the AO in 237 patients with HFrEF (10.0 ± 4.5 versus 10.5 ± 4.3 pmoL/mL, P < 0.0001) and were significantly higher in the CS than those in the AO (8.0 ± 3.6 versus 8.9 ± 3.8 pmoL/mL, P < 0.0001) in mild HF patients (New York Heart Association (NYHA) II, n = 114), but there was no difference in plasma cGMP between the AO and the CS (11.9 ± 4.4 versus 11.9 ± 4.3 pmoL/mL, NS) in severe HF patients (NYHA III-IV, n = 123). In mild HF patients, log (ANP + BNP) in the AO was an independent predictor of (CS-AO) cGMP among hemodynamics and nitrate therapy. There was a significant correlation between log [(CS-AO) ANP + (CS-AO) BNP] and (CS-AO) cGMP (r = 0.455, P < 0.0001) in mild HF patients.These findings indicate that cGMP is produced from the failing heart and that the heart is the target organ of endogenous ANP and BNP in patients with HFrEF. In severe HF patients, cGMP production may be attenuated because of the downregulation of biological receptors and/or increased cGMP degradation in the failing heart.
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