Cardiac Natriuretic Peptide Profiles in Chronic Hypertension by Single or Sequentially Combined Renovascular and DOCA-Salt Treatments

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 stu...

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Bibliographic Details
Authors: Cerrudo, Carolina Susana, Cavallero, Carmen Susana, Rodríguez Fermepin, Martin, González, Germán Esteban, Donato, Pablo Martín, Kouyoumdzian, Nicolás Martín, Gelpi, Ricardo Jorge, Hertig, Cecilia Margarita, Choi, Marcelo Roberto, Fernandez, Belisario Enrique
Format: article
Status:Published version
Publication Date:2021
Country:Argentina
Institution:Consejo Nacional de Investigaciones Científicas y Técnicas
Repository:CONICET Digital (CONICET)
Language:English
OAI Identifier:oai:ri.conicet.gov.ar:11336/182387
Online Access:http://hdl.handle.net/11336/182387
Access Level:Open access
Keyword:ATRIAL NATRIURETIC FACTOR
B TYPE NATRIURETIC PEPTIDE
CARDIAC HYPERTROPHY
DOCA-SALT HYPERTENSION
NATRIURETIC PEPTIDES SYSTEM
RAT MODELS
RENOVASCULAR HYPERTENSION
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Description
Summary: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.