Loading…

Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling

Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspr...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences 2022-01, Vol.23 (3), p.1233
Main Authors: Vieira-Rocha, Maria Sofia, Rodriguez-Rodriguez, Pilar, Ferreira-Duarte, Mariana, Faria, Miguel, Sousa, Joana Beatriz, Morato, Manuela, Arribas, Silvia Magdalena, Diniz, Carmen
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13
cites cdi_FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13
container_end_page
container_issue 3
container_start_page 1233
container_title International journal of molecular sciences
container_volume 23
creator Vieira-Rocha, Maria Sofia
Rodriguez-Rodriguez, Pilar
Ferreira-Duarte, Mariana
Faria, Miguel
Sousa, Joana Beatriz
Morato, Manuela
Arribas, Silvia Magdalena
Diniz, Carmen
description Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT receptors and NADPH oxidase, and lower expression of AT , Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension.
doi_str_mv 10.3390/ijms23031233
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8835999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2627635555</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13</originalsourceid><addsrcrecordid>eNpdkc9rFTEQx4MotlZvniXgxYNPk8z-SC5CfbYqVArVeg2z2dnXPHaTNtkt-t-bR2t5OpeZYT58mS9fxl5K8Q7AiPd-O2UFAqQCeMQOZaXUSoimfbw3H7BnOW-FUKBq85QdQC0bkLU-ZOMpzTjyy9BTCsuc_Oxj4N9i7wdPmf_E7JYRE784_s4_4ojBET8JV6X7sOHnv3yPs78l_gkn3BDH0PN1DEWnW-YdMUd-QVPsaSzbc_ZkwDHTi_t-xC5PT36sv6zOzj9_XR-frVwl1bzSgK6TgxY1IGLXIxjTIVUDDKJtq7YTTrfQtLVUnapI9p2Tchi0JoFVhRKO2Ic73eulm6h3VB7C0V4nP2H6bSN6--8l-Cu7ibdWa6iNMUXgzb1AijcL5dlOPjsai3-KS7aqUUbUujJQ0Nf_odu4pFDs7ai2gbpUod7eUS7FnBMND89IYXcx2v0YC_5q38AD_Dc3-AMN5pp4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2627635555</pqid></control><display><type>article</type><title>Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Vieira-Rocha, Maria Sofia ; Rodriguez-Rodriguez, Pilar ; Ferreira-Duarte, Mariana ; Faria, Miguel ; Sousa, Joana Beatriz ; Morato, Manuela ; Arribas, Silvia Magdalena ; Diniz, Carmen</creator><creatorcontrib>Vieira-Rocha, Maria Sofia ; Rodriguez-Rodriguez, Pilar ; Ferreira-Duarte, Mariana ; Faria, Miguel ; Sousa, Joana Beatriz ; Morato, Manuela ; Arribas, Silvia Magdalena ; Diniz, Carmen</creatorcontrib><description>Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT receptors and NADPH oxidase, and lower expression of AT , Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23031233</identifier><identifier>PMID: 35163158</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Arteries ; Blood Pressure ; Carbonyl compounds ; Carbonyls ; Cardiovascular diseases ; Endocrine system ; Enzymes ; Female ; Fetal Development ; Fetal Nutrition Disorders - physiopathology ; Fetuses ; Hypertension ; Immunohistochemistry ; Male ; Maternal Nutritional Physiological Phenomena ; Mesenteric Arteries - metabolism ; Mesenteric Arteries - pathology ; Morphology ; NAD(P)H oxidase ; Nitric oxide ; Oxidative Stress ; Peptides ; Physiology ; Plasma ; Plasma levels ; Rats ; Rats, Sprague-Dawley ; Receptor, Angiotensin, Type 1 - genetics ; Receptor, Angiotensin, Type 1 - metabolism ; Receptor, Angiotensin, Type 2 - genetics ; Receptor, Angiotensin, Type 2 - metabolism ; Renin-Angiotensin System ; Rodents ; Spectrophotometry ; Undernutrition ; Vascular Remodeling ; Veins &amp; arteries</subject><ispartof>International journal of molecular sciences, 2022-01, Vol.23 (3), p.1233</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13</citedby><cites>FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13</cites><orcidid>0000-0003-4668-9360 ; 0000-0002-9509-0613</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2627635555/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2627635555?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,36992,44569,53769,53771,74872</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35163158$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vieira-Rocha, Maria Sofia</creatorcontrib><creatorcontrib>Rodriguez-Rodriguez, Pilar</creatorcontrib><creatorcontrib>Ferreira-Duarte, Mariana</creatorcontrib><creatorcontrib>Faria, Miguel</creatorcontrib><creatorcontrib>Sousa, Joana Beatriz</creatorcontrib><creatorcontrib>Morato, Manuela</creatorcontrib><creatorcontrib>Arribas, Silvia Magdalena</creatorcontrib><creatorcontrib>Diniz, Carmen</creatorcontrib><title>Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT receptors and NADPH oxidase, and lower expression of AT , Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension.</description><subject>Animals</subject><subject>Arteries</subject><subject>Blood Pressure</subject><subject>Carbonyl compounds</subject><subject>Carbonyls</subject><subject>Cardiovascular diseases</subject><subject>Endocrine system</subject><subject>Enzymes</subject><subject>Female</subject><subject>Fetal Development</subject><subject>Fetal Nutrition Disorders - physiopathology</subject><subject>Fetuses</subject><subject>Hypertension</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Maternal Nutritional Physiological Phenomena</subject><subject>Mesenteric Arteries - metabolism</subject><subject>Mesenteric Arteries - pathology</subject><subject>Morphology</subject><subject>NAD(P)H oxidase</subject><subject>Nitric oxide</subject><subject>Oxidative Stress</subject><subject>Peptides</subject><subject>Physiology</subject><subject>Plasma</subject><subject>Plasma levels</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Angiotensin, Type 1 - genetics</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Receptor, Angiotensin, Type 2 - genetics</subject><subject>Receptor, Angiotensin, Type 2 - metabolism</subject><subject>Renin-Angiotensin System</subject><subject>Rodents</subject><subject>Spectrophotometry</subject><subject>Undernutrition</subject><subject>Vascular Remodeling</subject><subject>Veins &amp; arteries</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkc9rFTEQx4MotlZvniXgxYNPk8z-SC5CfbYqVArVeg2z2dnXPHaTNtkt-t-bR2t5OpeZYT58mS9fxl5K8Q7AiPd-O2UFAqQCeMQOZaXUSoimfbw3H7BnOW-FUKBq85QdQC0bkLU-ZOMpzTjyy9BTCsuc_Oxj4N9i7wdPmf_E7JYRE784_s4_4ojBET8JV6X7sOHnv3yPs78l_gkn3BDH0PN1DEWnW-YdMUd-QVPsaSzbc_ZkwDHTi_t-xC5PT36sv6zOzj9_XR-frVwl1bzSgK6TgxY1IGLXIxjTIVUDDKJtq7YTTrfQtLVUnapI9p2Tchi0JoFVhRKO2Ic73eulm6h3VB7C0V4nP2H6bSN6--8l-Cu7ibdWa6iNMUXgzb1AijcL5dlOPjsai3-KS7aqUUbUujJQ0Nf_odu4pFDs7ai2gbpUod7eUS7FnBMND89IYXcx2v0YC_5q38AD_Dc3-AMN5pp4</recordid><startdate>20220122</startdate><enddate>20220122</enddate><creator>Vieira-Rocha, Maria Sofia</creator><creator>Rodriguez-Rodriguez, Pilar</creator><creator>Ferreira-Duarte, Mariana</creator><creator>Faria, Miguel</creator><creator>Sousa, Joana Beatriz</creator><creator>Morato, Manuela</creator><creator>Arribas, Silvia Magdalena</creator><creator>Diniz, Carmen</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4668-9360</orcidid><orcidid>https://orcid.org/0000-0002-9509-0613</orcidid></search><sort><creationdate>20220122</creationdate><title>Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling</title><author>Vieira-Rocha, Maria Sofia ; Rodriguez-Rodriguez, Pilar ; Ferreira-Duarte, Mariana ; Faria, Miguel ; Sousa, Joana Beatriz ; Morato, Manuela ; Arribas, Silvia Magdalena ; Diniz, Carmen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Arteries</topic><topic>Blood Pressure</topic><topic>Carbonyl compounds</topic><topic>Carbonyls</topic><topic>Cardiovascular diseases</topic><topic>Endocrine system</topic><topic>Enzymes</topic><topic>Female</topic><topic>Fetal Development</topic><topic>Fetal Nutrition Disorders - physiopathology</topic><topic>Fetuses</topic><topic>Hypertension</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Maternal Nutritional Physiological Phenomena</topic><topic>Mesenteric Arteries - metabolism</topic><topic>Mesenteric Arteries - pathology</topic><topic>Morphology</topic><topic>NAD(P)H oxidase</topic><topic>Nitric oxide</topic><topic>Oxidative Stress</topic><topic>Peptides</topic><topic>Physiology</topic><topic>Plasma</topic><topic>Plasma levels</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Receptor, Angiotensin, Type 2 - genetics</topic><topic>Receptor, Angiotensin, Type 2 - metabolism</topic><topic>Renin-Angiotensin System</topic><topic>Rodents</topic><topic>Spectrophotometry</topic><topic>Undernutrition</topic><topic>Vascular Remodeling</topic><topic>Veins &amp; arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vieira-Rocha, Maria Sofia</creatorcontrib><creatorcontrib>Rodriguez-Rodriguez, Pilar</creatorcontrib><creatorcontrib>Ferreira-Duarte, Mariana</creatorcontrib><creatorcontrib>Faria, Miguel</creatorcontrib><creatorcontrib>Sousa, Joana Beatriz</creatorcontrib><creatorcontrib>Morato, Manuela</creatorcontrib><creatorcontrib>Arribas, Silvia Magdalena</creatorcontrib><creatorcontrib>Diniz, Carmen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vieira-Rocha, Maria Sofia</au><au>Rodriguez-Rodriguez, Pilar</au><au>Ferreira-Duarte, Mariana</au><au>Faria, Miguel</au><au>Sousa, Joana Beatriz</au><au>Morato, Manuela</au><au>Arribas, Silvia Magdalena</au><au>Diniz, Carmen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2022-01-22</date><risdate>2022</risdate><volume>23</volume><issue>3</issue><spage>1233</spage><pages>1233-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT receptors and NADPH oxidase, and lower expression of AT , Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>35163158</pmid><doi>10.3390/ijms23031233</doi><orcidid>https://orcid.org/0000-0003-4668-9360</orcidid><orcidid>https://orcid.org/0000-0002-9509-0613</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1422-0067
ispartof International journal of molecular sciences, 2022-01, Vol.23 (3), p.1233
issn 1422-0067
1661-6596
1422-0067
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8835999
source Publicly Available Content Database; PubMed Central
subjects Animals
Arteries
Blood Pressure
Carbonyl compounds
Carbonyls
Cardiovascular diseases
Endocrine system
Enzymes
Female
Fetal Development
Fetal Nutrition Disorders - physiopathology
Fetuses
Hypertension
Immunohistochemistry
Male
Maternal Nutritional Physiological Phenomena
Mesenteric Arteries - metabolism
Mesenteric Arteries - pathology
Morphology
NAD(P)H oxidase
Nitric oxide
Oxidative Stress
Peptides
Physiology
Plasma
Plasma levels
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 - genetics
Receptor, Angiotensin, Type 1 - metabolism
Receptor, Angiotensin, Type 2 - genetics
Receptor, Angiotensin, Type 2 - metabolism
Renin-Angiotensin System
Rodents
Spectrophotometry
Undernutrition
Vascular Remodeling
Veins & arteries
title Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-25T18%3A37%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Fetal%20Undernutrition%20Modifies%20Vascular%20RAS%20Balance%20Enhancing%20Oxidative%20Damage%20and%20Contributing%20to%20Remodeling&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Vieira-Rocha,%20Maria%20Sofia&rft.date=2022-01-22&rft.volume=23&rft.issue=3&rft.spage=1233&rft.pages=1233-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23031233&rft_dat=%3Cproquest_pubme%3E2627635555%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c412t-83acb1f8053aaabda399bae4f3f07747b0c87367512b24e1dbc11ff88e0a44a13%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2627635555&rft_id=info:pmid/35163158&rfr_iscdi=true