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Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and
Carolina S Cerrudo1, Susana Cavallero1, Martín Rodríguez Fermepín1
1Facultad de Farmacia y Bioquímica, Cátedras de Fisiopatología y Anatomía e Histología, Universidad de Buenos Aires, Buenos Aires, Argentina.
Insights
Natriuretic peptides like ANP and BNP show differential gene expression during cardiac remodeling. Volume overload impacts ANP more, while pressure overload affects BNP in hypertrophied ventricles.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
Background:
- Chronic hemodynamic overload induces cardiac hypertrophy and remodeling.
- Natriuretic peptides, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), play roles in cardiovascular homeostasis.
- Understanding the differential regulation of ANP and BNP during distinct overload conditions is crucial for cardiovascular research.
Purpose of the Study:
- To investigate the involvement of natriuretic peptides during hypertrophic remodeling.
- To compare the effects of pressure overload (renovascular hypertension) and volume overload (DOCA-salt) on cardiac hypertrophy and natriuretic peptide gene expression.
- To examine the impact of sequential combined overload models on these parameters.
Main Methods:
- Induction of hypertension in rats using renovascular (pressure overload) and DOCA-salt (volume overload) models for 6 and 12 weeks.
- Assessment of cardiac hypertrophy and left ventricular ANP and BNP gene expression.
- Evaluation of combined sequential overload models (RV/DS and DS/RV).
Main Results:
- Both single and combined overload models induced hypertension and cardiac hypertrophy.
- Cardiac hypertrophy and ANP gene expression were more pronounced in the DOCA-salt (volume overload) group compared to the renovascular (pressure overload) group.
- BNP gene expression correlated with hypertrophy in pressure overload, while ANP correlated with hypertrophy in volume overload.
- Sequential combined overload showed intermediate effects, with the second stimulus being less potent than the first.
Conclusions:
- Volume and pressure overload differentially regulate ANP and BNP gene expression in hypertrophied left ventricles.
- ANP synthesis is suggested to correlate with volume overload, while BNP synthesis correlates with pressure overload-induced hypertrophy.
- Plasma ANP levels reflect volume changes, whereas circulating BNP levels are linked to cardiac synthesis and ventricular hypertrophy.
Abstract:
The involvement of natriuretic peptides was studied during the hypertrophic remodeling transition mediated by sequential exposure to chronic hemodynamic overload. We induced hypertension in rats by pressure (renovascular) or volume overload (DOCA-salt) during 6 and 12 weeks of treatment. We also studied the consecutive combination of both models in inverse sequences: RV 6 weeks/DS 6 weeks and DS 6 weeks/RV 6 weeks. All treated groups developed hypertension. Cardiac hypertrophy and left ventricular ANP gene expression were more pronounced in single DS than in single RV groups. BNP gene expression was positively correlated with left ventricular hypertrophy only in RV groups, while ANP gene expression was positively correlated with left ventricular hypertrophy only in DS groups. Combined models exhibited intermediate values between those of single groups at 6 and 12 weeks. The latter stimulus associated to the second applied overload is less effective than the former to trigger cardiac hypertrophy and to increase ANP and BNP gene expression. In addition, we suggest a correlation of ANP synthesis with volume overload and of BNP synthesis with pressure overload-induced hypertrophy after a prolonged treatment. Volume and pressure overload may be two mechanisms, among others, involved in the differential regulation of ANP and BNP gene expression in hypertrophied left ventricles. Plasma ANP levels reflect a response to plasma volume increase and volume overload, while circulating BNP levels seem to be regulated by cardiac BNP synthesis and ventricular hypertrophy.
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