Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition

Fetal undernutrition is a risk factor for cardiovascular diseases. Male offspring from rats exposed to undernutrition during gestation (MUN) exhibit oxidative stress during perinatal life and develop cardiac dysfunction in ageing. Angiotensin-II is implicated in oxidative stress-mediated cardiovascu...

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Authors: Rodríguez Rodríguez, Pilar, Vieira Rocha, Maria Sofía, Quintana Villamandos, María Begoña, Monedero Cobeta, Ignacio, Prachaney, Parichat, López de Pablo, Angel Luis, González, Maria del Carmen, Morato, Manuela, Diniz, Carmen, Arribas, Silvia M.
Format: article
Publication Date:2021
Country:España
Institution:Universidad Complutense de Madrid (UCM)
Repository:Docta Complutense
Language:English
OAI Identifier:oai:docta.ucm.es:20.500.14352/7134
Online Access:https://hdl.handle.net/20.500.14352/7134
Access Level:Open access
Keyword:angiotensin II
fetal programming
fibrosis
lactation
left ventricular hypertrophy
cardiovascular remodeling
RAS receptors
Ginecología y obstetricia
3201.08 Ginecología
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spelling Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal UndernutritionRodríguez Rodríguez, PilarVieira Rocha, Maria SofíaQuintana Villamandos, María BegoñaMonedero Cobeta, IgnacioPrachaney, ParichatLópez de Pablo, Angel LuisGonzález, Maria del CarmenMorato, ManuelaDiniz, CarmenArribas, Silvia M.angiotensin IIfetal programmingfibrosislactationleft ventricular hypertrophycardiovascular remodelingRAS receptorsGinecología y obstetricia3201.08 GinecologíaFetal undernutrition is a risk factor for cardiovascular diseases. Male offspring from rats exposed to undernutrition during gestation (MUN) exhibit oxidative stress during perinatal life and develop cardiac dysfunction in ageing. Angiotensin-II is implicated in oxidative stress-mediated cardiovascular fibrosis and remodeling, and lactation is a key developmental window. We aimed to assess if alterations in RAS during lactation participate in cardiac dysfunction associated with fetal undernutrition. Control dams received food ad libitum, and MUN had 50% nutrient restriction during the second half of gestation. Both dams were fed ad libitum during lactation, and male offspring were studied at weaning. We assessed: ventricular structure and function (echocardiography); blood pressure (intra-arterially, anesthetized rats); collagen content and intramyocardial artery structure (Sirius red, Masson Trichromic); myocardial and intramyocardial artery RAS receptors (immunohistochemistry); plasma angiotensin-II (ELISA) and TGF-β1 protein expression (Western Blot). Compared to Control, MUN offspring exhibited significantly higher plasma Angiotensin-II and a larger left ventricular mass, as well as larger intramyocardial artery media/lumen, interstitial collagen and perivascular collagen. In MUN hearts, TGF-β1 tended to be higher, and the end-diastolic diameter and E/A ratio were significantly lower with no differences in ejection fraction or blood pressure. In the myocardium, no differences between groups were detected in AT1, AT2 or Mas receptors, with MrgD being significantly lower in the MUN group. In intramyocardial arteries from MUN rats, AT1 and Mas receptors were significantly elevated, while AT2 and MrgD were lower compared to Control. Conclusions. In rats exposed to fetal undernutrition, RAS disbalance and associated cardiac remodeling during lactation may set the basis for later heart dysfunction.MPDIUniversidad Complutense de Madrid20212021-06-0520212021-06-05journal articlehttp://purl.org/coar/resource_type/c_6501info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.14352/7134reponame:Docta Complutenseinstname:Universidad Complutense de Madrid (UCM)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución 3.0 Españahttps://creativecommons.org/licenses/by/3.0/es/info:eu-repo/semantics/openAccessoai:docta.ucm.es:20.500.14352/71342026-06-02T12:44:21Z
dc.title.none.fl_str_mv Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
title Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
spellingShingle Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
Rodríguez Rodríguez, Pilar
angiotensin II
fetal programming
fibrosis
lactation
left ventricular hypertrophy
cardiovascular remodeling
RAS receptors
Ginecología y obstetricia
3201.08 Ginecología
title_short Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
title_full Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
title_fullStr Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
title_full_unstemmed Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
title_sort Implication of RAS in Postnatal Cardiac Remodeling, Fibrosis and Dysfunction Induced by Fetal Undernutrition
dc.creator.none.fl_str_mv Rodríguez Rodríguez, Pilar
Vieira Rocha, Maria Sofía
Quintana Villamandos, María Begoña
Monedero Cobeta, Ignacio
Prachaney, Parichat
López de Pablo, Angel Luis
González, Maria del Carmen
Morato, Manuela
Diniz, Carmen
Arribas, Silvia M.
author Rodríguez Rodríguez, Pilar
author_facet Rodríguez Rodríguez, Pilar
Vieira Rocha, Maria Sofía
Quintana Villamandos, María Begoña
Monedero Cobeta, Ignacio
Prachaney, Parichat
López de Pablo, Angel Luis
González, Maria del Carmen
Morato, Manuela
Diniz, Carmen
Arribas, Silvia M.
author_role author
author2 Vieira Rocha, Maria Sofía
Quintana Villamandos, María Begoña
Monedero Cobeta, Ignacio
Prachaney, Parichat
López de Pablo, Angel Luis
González, Maria del Carmen
Morato, Manuela
Diniz, Carmen
Arribas, Silvia M.
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad Complutense de Madrid
dc.subject.none.fl_str_mv angiotensin II
fetal programming
fibrosis
lactation
left ventricular hypertrophy
cardiovascular remodeling
RAS receptors
Ginecología y obstetricia
3201.08 Ginecología
topic angiotensin II
fetal programming
fibrosis
lactation
left ventricular hypertrophy
cardiovascular remodeling
RAS receptors
Ginecología y obstetricia
3201.08 Ginecología
description Fetal undernutrition is a risk factor for cardiovascular diseases. Male offspring from rats exposed to undernutrition during gestation (MUN) exhibit oxidative stress during perinatal life and develop cardiac dysfunction in ageing. Angiotensin-II is implicated in oxidative stress-mediated cardiovascular fibrosis and remodeling, and lactation is a key developmental window. We aimed to assess if alterations in RAS during lactation participate in cardiac dysfunction associated with fetal undernutrition. Control dams received food ad libitum, and MUN had 50% nutrient restriction during the second half of gestation. Both dams were fed ad libitum during lactation, and male offspring were studied at weaning. We assessed: ventricular structure and function (echocardiography); blood pressure (intra-arterially, anesthetized rats); collagen content and intramyocardial artery structure (Sirius red, Masson Trichromic); myocardial and intramyocardial artery RAS receptors (immunohistochemistry); plasma angiotensin-II (ELISA) and TGF-β1 protein expression (Western Blot). Compared to Control, MUN offspring exhibited significantly higher plasma Angiotensin-II and a larger left ventricular mass, as well as larger intramyocardial artery media/lumen, interstitial collagen and perivascular collagen. In MUN hearts, TGF-β1 tended to be higher, and the end-diastolic diameter and E/A ratio were significantly lower with no differences in ejection fraction or blood pressure. In the myocardium, no differences between groups were detected in AT1, AT2 or Mas receptors, with MrgD being significantly lower in the MUN group. In intramyocardial arteries from MUN rats, AT1 and Mas receptors were significantly elevated, while AT2 and MrgD were lower compared to Control. Conclusions. In rats exposed to fetal undernutrition, RAS disbalance and associated cardiac remodeling during lactation may set the basis for later heart dysfunction.
publishDate 2021
dc.date.none.fl_str_mv 2021
2021-06-05
2021
2021-06-05
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv https://hdl.handle.net/20.500.14352/7134
url https://hdl.handle.net/20.500.14352/7134
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
https://creativecommons.org/licenses/by/3.0/es/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
https://creativecommons.org/licenses/by/3.0/es/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv MPDI
publisher.none.fl_str_mv MPDI
dc.source.none.fl_str_mv reponame:Docta Complutense
instname:Universidad Complutense de Madrid (UCM)
instname_str Universidad Complutense de Madrid (UCM)
reponame_str Docta Complutense
collection Docta Complutense
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300719

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