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Updated: May 4, 2026
Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
Atrial natriuretic peptide affects cardiac remodeling, function, heart failure, and survival in a mouse model of
Dong Wang1, Inna P Gladysheva, Tai-Hwang M Fan
1Department of Medicine, University of Tennessee Health Science Center, Coleman, D334, 956 Court Ave, Memphis, TN 38163. glreed@uthsc.edu.
Insights
Atrial natriuretic peptide (ANP) protects against heart failure in dilated cardiomyopathy. Normal ANP levels improve cardiac function, reduce remodeling, and increase survival, demonstrating ANP
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Dilated cardiomyopathy (DCM) is a significant cause of heart failure and mortality.
- Atrial natriuretic peptide (ANP) is a known biomarker for DCM, but its role in disease progression remains debated.
- Understanding ANP's influence is crucial for developing targeted therapies for heart failure.
Purpose of the Study:
- To investigate the specific effects of Atrial natriuretic peptide (ANP) on heart failure development, cardiac remodeling, function, and survival in a transgenic mouse model of dilated cardiomyopathy (DCM).
- To determine if ANP levels modulate the progression of heart failure and associated pathological changes in DCM.
- To explore the compensatory roles of other natriuretic peptides (NPs) in the context of ANP deficiency in DCM.
Main Methods:
- Utilized a well-characterized transgenic mouse model of dilated cardiomyopathy (DCM).
- Compared survival rates, cardiac function, and pathological remodeling in DCM mice with normal ANP levels versus those with partial or full ANP deficiency.
- Assessed physiological markers of heart failure (e.g., lung water, effusions) and cardiac fibrosis.
- Quantified cardiac gene expression for natriuretic peptide receptors (NPRA, NPRB, NPRC) and C-type natriuretic peptide (CNP).
Main Results:
- Mice with dilated cardiomyopathy (DCM) and normal Atrial natriuretic peptide (ANP) levels exhibited significantly longer survival compared to those with ANP deficiency.
- ANP demonstrated protective effects against heart failure development in DCM, evidenced by reduced lung congestion and improved systolic function.
- Pathological cardiac remodeling, including ventricular fibrosis, was significantly diminished in DCM mice with normal ANP levels.
- Gene expression analysis revealed altered natriuretic peptide receptor (NPR) and C-type natriuretic peptide (CNP) transcripts in DCM mice with ANP deficiency.
Conclusions:
- Atrial natriuretic peptide (ANP) exerts potent protective effects in experimental dilated cardiomyopathy (DCM), mitigating heart failure, preventing adverse remodeling, preserving systolic function, and reducing mortality.
- These findings indicate that ANP plays a critical role in managing DCM progression.
- The study suggests that other natriuretic peptides (NPs) do not fully compensate for the loss of ANP's function in the context of DCM and heart failure.
Abstract:
Dilated cardiomyopathy is a frequent cause of heart failure and death. Atrial natriuretic peptide (ANP) is a biomarker of dilated cardiomyopathy, but there is controversy whether ANP modulates the development of heart failure. Therefore, we examined whether ANP affects heart failure, cardiac remodeling, function, and survival in a well-characterized, transgenic model of dilated cardiomyopathy. Mice with dilated cardiomyopathy with normal ANP levels survived longer than mice with partial ANP (P<0.01) or full ANP deficiency (P<0.001). In dilated cardiomyopathy mice, ANP protected against the development of heart failure as indicated by reduced lung water, alveolar congestion, pleural effusions, etc. ANP improved systolic function and reduced cardiomegaly. Pathological cardiac remodeling was diminished in mice with normal ANP as indicated by decreased ventricular interstitial and perivascular fibrosis. Mice with dilated cardiomyopathy and normal ANP levels had better systolic function (P<0.001) than mice with dilated cardiomyopathy and ANP deficiency. Dilated cardiomyopathy was associated with diminished cardiac transcripts for NP receptors A and B in mice with normal ANP and ANP deficiency, but transcripts for NP receptor C and C-type natriuretic peptide were selectively altered in mice with dilated cardiomyopathy and ANP deficiency. Taken together, these data indicate that ANP has potent effects in experimental dilated cardiomyopathy that reduce the development of heart failure, prevent pathological remodeling, preserve systolic function, and reduce mortality. Despite the apparent overlap in physiological function between the NPs, these data suggest that the role of ANP in dilated cardiomyopathy and heart failure is not compensated physiologically by other NPs.
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