Related Experiment Video
Updated: Jun 22, 2026

Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
Asymmetrical myocardial expression of natriuretic peptides in pacing-induced heart failure
Silvia Del Ry1, Manuela Cabiati, Vincenzo Lionetti
1CNR Institute of Clinical Physiology and G. Monasterio Foundation-CNR Regione Toscana, Via Giuseppe Moruzzi 1, Pisa, Italy. delry@ifc.cnr.it
Insights
High-frequency pacing induces heart failure with regional contractility differences. Brain natriuretic peptide (BNP) mRNA increased at the pacing site, while C-type natriuretic peptide (CNP) expression rose in remote areas, suggesting regional dysfunction.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Left ventricular (LV) free wall pacing induces dyssynchronous contraction, leading to heart failure (HF).
- Regional differences in contractility are pronounced in pacing-induced HF.
- Brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are key biomarkers in cardiovascular disease.
Purpose of the Study:
- To evaluate changes in BNP and CNP mRNA expression in pacing-induced HF minipigs.
- To compare biomarker expression between the pacing site (PS) and the opposite site (OS).
- To explore associations between regional contractility patterns and biomarker expression.
Main Methods:
- Cardiac tissue samples were collected from minipigs with (n=8) and without (n=6) pacing-induced HF.
- Tissue was harvested from the anterior LV wall (PS) and the infero-septal region (OS).
- Semi-quantitative polymerase chain reaction (PCR) was used to assess BNP and CNP mRNA expression.
Main Results:
- BNP mRNA expression was significantly higher at the PS in HF animals compared to controls (p=0.02).
- No significant difference in BNP mRNA was observed at the OS.
- CNP mRNA expression and tissue concentration were elevated at both PS and OS in HF animals, particularly at the OS (p=0.039).
Conclusions:
- Increased BNP mRNA at the PS correlates with reduced contractile function in the paced region.
- Elevated CNP mRNA and concentration at the OS suggest concomitant endothelial dysfunction in remote myocardial areas.
- These findings highlight regional molecular adaptations in pacing-induced heart failure.
Abstract:
High-frequency pacing of the left ventricle (LV) free wall causes a dyssynchronous pattern of contraction that leads to progressive heart failure (HF) with pronounced differences in regional contractility. Aim of this study was to evaluate possible changes in brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) mRNA expression in the anterior/anterior lateral region (pacing site, PS) as compared to the infero-septal region (opposite site, OS) and to explore possible association between the contractiling pattern and biomarker expression. Cardiac tissue was collected from minipigs with pacing-induced HF (n=8) and without (control, n=6). The samples were selectively harvested from the anterior left ventricular (LV) wall, PS, and from an area remote to the pacing-site, OS. BNP and CNP mRNA expression was evaluated by semi-quantitative polymerase chain reaction (PCR). A significant difference in BNP expression was found in the PS between HF animals and controls (BNP/GAPDH: 0.65+/-0.11 vs. 0.35+/-0.04, p=0.02), but not in the OS (BNP/GAPDH: 0.36+/-0.05, ns vs. controls). CNP expression was not different compared to controls, although higher levels were observed in the PS and in the OS with respect to the controls (CNP/GAPDH: controls 0.089+/-0.036, PS 0.289+/-0.23, OS 0.54+/-0.16). This finding was in tune with an increase of CNP tissue concentration (controls: 0.69+/-0.13; PS=1.56+/-0.19; OS=1.70+/-0.42 pg/mg protein; p=0.039 controls vs. OS). Higher BNP mRNA expression in the PS is consistent with a reduction in contractile function in this region, while higher CNP mRNA expression in the OS suggests the presence of concomitant endothelial dysfunction in the remote region.
Related Concept Videos
Heart Failure II: Pathophysiology
Pathophysiology of Heart Failure
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Heart Failure Drugs: Diuretics
Cardiomyopathy II: Dilated Cardiomyopathy
Heart Failure Drugs: Inotropic Agents
