Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors

Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Experimental eye research 2020-04, Vol.193, p.107981-107981, Article 107981
Hauptverfasser: Ramírez-Montero, Claudia, Lima-Gómez, Virgilio, Anguiano-Robledo, Liliana, Hernández-Campos, María Elena, López-Sánchez, Pedro
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 107981
container_issue
container_start_page 107981
container_title Experimental eye research
container_volume 193
creator Ramírez-Montero, Claudia
Lima-Gómez, Virgilio
Anguiano-Robledo, Liliana
Hernández-Campos, María Elena
López-Sánchez, Pedro
description Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation. •AT1 receptor and (Pro)renin/renin receptor participates in preeclampsia retinopathy.•VEGF and PEDF are augmented in preeclamptic retinopathy.•L-NAME-induced hypertension develops faster in previously preeclamptic animals.•AT1 receptor and (Pro)renin/renin receptor participate in L-NAME-induced retinopathy.•VEGF and PEDF do not seem to participate in L-NAME-induced retinopathy.
doi_str_mv 10.1016/j.exer.2020.107981
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2363090242</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0014483519308474</els_id><sourcerecordid>2363090242</sourcerecordid><originalsourceid>FETCH-LOGICAL-c356t-5a842f7bfe4d7597af0126909b723b6416380522d8fd3e9592df89d33cb019093</originalsourceid><addsrcrecordid>eNp9kE2LUzEUhoMoTh39Ay4kSze3nnzcj4ibMqgzMODgxzrkJidtSntzTdJh-u9NaXXp4hByeN4XzkPIWwZLBqz7sF3iE6YlB35a9Gpgz8iCgeoaAOifkwUAk40cRHtFXuW8rVshe_mSXAkOw8AlLEh6SIh2Z_ZzDoaaTOeELuQ55jCtqTe2xER9nc1xxlRwyuERacISpjibsjl-pA8mlWBD_YU40fFIywbp99XqBzWTq7MOcY1TsJe2_Jq88GaX8c3lvSa_vnz-eXPb3H_7enezum-saLvStGaQ3PejR-n6VvXGA-OdAjX2XIydZJ0YoOXcDd4JVK3izg_KCWFHYBUT1-T9uXdO8fcBc9H7kC3udmbCeMiai06AAi55RfkZtSnmnNDrOYW9SUfNQJ9c660-udYn1_rsuobeXfoP4x7dv8hfuRX4dAawXvkYajzbgJOtghPaol0M_-v_Axy2kMk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2363090242</pqid></control><display><type>article</type><title>Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors</title><source>Elsevier ScienceDirect Journals</source><creator>Ramírez-Montero, Claudia ; Lima-Gómez, Virgilio ; Anguiano-Robledo, Liliana ; Hernández-Campos, María Elena ; López-Sánchez, Pedro</creator><creatorcontrib>Ramírez-Montero, Claudia ; Lima-Gómez, Virgilio ; Anguiano-Robledo, Liliana ; Hernández-Campos, María Elena ; López-Sánchez, Pedro</creatorcontrib><description>Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation. •AT1 receptor and (Pro)renin/renin receptor participates in preeclampsia retinopathy.•VEGF and PEDF are augmented in preeclamptic retinopathy.•L-NAME-induced hypertension develops faster in previously preeclamptic animals.•AT1 receptor and (Pro)renin/renin receptor participate in L-NAME-induced retinopathy.•VEGF and PEDF do not seem to participate in L-NAME-induced retinopathy.</description><identifier>ISSN: 0014-4835</identifier><identifier>EISSN: 1096-0007</identifier><identifier>DOI: 10.1016/j.exer.2020.107981</identifier><identifier>PMID: 32088240</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>(Pro) renin/renin receptor ; AT1 receptor ; Hypertension ; PEDF ; Preeclampsia ; Pregnancy ; Retinopathy ; VEGF</subject><ispartof>Experimental eye research, 2020-04, Vol.193, p.107981-107981, Article 107981</ispartof><rights>2020 Elsevier Ltd</rights><rights>Copyright © 2020 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-5a842f7bfe4d7597af0126909b723b6416380522d8fd3e9592df89d33cb019093</citedby><cites>FETCH-LOGICAL-c356t-5a842f7bfe4d7597af0126909b723b6416380522d8fd3e9592df89d33cb019093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014483519308474$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32088240$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ramírez-Montero, Claudia</creatorcontrib><creatorcontrib>Lima-Gómez, Virgilio</creatorcontrib><creatorcontrib>Anguiano-Robledo, Liliana</creatorcontrib><creatorcontrib>Hernández-Campos, María Elena</creatorcontrib><creatorcontrib>López-Sánchez, Pedro</creatorcontrib><title>Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors</title><title>Experimental eye research</title><addtitle>Exp Eye Res</addtitle><description>Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation. •AT1 receptor and (Pro)renin/renin receptor participates in preeclampsia retinopathy.•VEGF and PEDF are augmented in preeclamptic retinopathy.•L-NAME-induced hypertension develops faster in previously preeclamptic animals.•AT1 receptor and (Pro)renin/renin receptor participate in L-NAME-induced retinopathy.•VEGF and PEDF do not seem to participate in L-NAME-induced retinopathy.</description><subject>(Pro) renin/renin receptor</subject><subject>AT1 receptor</subject><subject>Hypertension</subject><subject>PEDF</subject><subject>Preeclampsia</subject><subject>Pregnancy</subject><subject>Retinopathy</subject><subject>VEGF</subject><issn>0014-4835</issn><issn>1096-0007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kE2LUzEUhoMoTh39Ay4kSze3nnzcj4ibMqgzMODgxzrkJidtSntzTdJh-u9NaXXp4hByeN4XzkPIWwZLBqz7sF3iE6YlB35a9Gpgz8iCgeoaAOifkwUAk40cRHtFXuW8rVshe_mSXAkOw8AlLEh6SIh2Z_ZzDoaaTOeELuQ55jCtqTe2xER9nc1xxlRwyuERacISpjibsjl-pA8mlWBD_YU40fFIywbp99XqBzWTq7MOcY1TsJe2_Jq88GaX8c3lvSa_vnz-eXPb3H_7enezum-saLvStGaQ3PejR-n6VvXGA-OdAjX2XIydZJ0YoOXcDd4JVK3izg_KCWFHYBUT1-T9uXdO8fcBc9H7kC3udmbCeMiai06AAi55RfkZtSnmnNDrOYW9SUfNQJ9c660-udYn1_rsuobeXfoP4x7dv8hfuRX4dAawXvkYajzbgJOtghPaol0M_-v_Axy2kMk</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Ramírez-Montero, Claudia</creator><creator>Lima-Gómez, Virgilio</creator><creator>Anguiano-Robledo, Liliana</creator><creator>Hernández-Campos, María Elena</creator><creator>López-Sánchez, Pedro</creator><general>Elsevier Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202004</creationdate><title>Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors</title><author>Ramírez-Montero, Claudia ; Lima-Gómez, Virgilio ; Anguiano-Robledo, Liliana ; Hernández-Campos, María Elena ; López-Sánchez, Pedro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-5a842f7bfe4d7597af0126909b723b6416380522d8fd3e9592df89d33cb019093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>(Pro) renin/renin receptor</topic><topic>AT1 receptor</topic><topic>Hypertension</topic><topic>PEDF</topic><topic>Preeclampsia</topic><topic>Pregnancy</topic><topic>Retinopathy</topic><topic>VEGF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ramírez-Montero, Claudia</creatorcontrib><creatorcontrib>Lima-Gómez, Virgilio</creatorcontrib><creatorcontrib>Anguiano-Robledo, Liliana</creatorcontrib><creatorcontrib>Hernández-Campos, María Elena</creatorcontrib><creatorcontrib>López-Sánchez, Pedro</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental eye research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ramírez-Montero, Claudia</au><au>Lima-Gómez, Virgilio</au><au>Anguiano-Robledo, Liliana</au><au>Hernández-Campos, María Elena</au><au>López-Sánchez, Pedro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors</atitle><jtitle>Experimental eye research</jtitle><addtitle>Exp Eye Res</addtitle><date>2020-04</date><risdate>2020</risdate><volume>193</volume><spage>107981</spage><epage>107981</epage><pages>107981-107981</pages><artnum>107981</artnum><issn>0014-4835</issn><eissn>1096-0007</eissn><abstract>Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation. •AT1 receptor and (Pro)renin/renin receptor participates in preeclampsia retinopathy.•VEGF and PEDF are augmented in preeclamptic retinopathy.•L-NAME-induced hypertension develops faster in previously preeclamptic animals.•AT1 receptor and (Pro)renin/renin receptor participate in L-NAME-induced retinopathy.•VEGF and PEDF do not seem to participate in L-NAME-induced retinopathy.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>32088240</pmid><doi>10.1016/j.exer.2020.107981</doi><tpages>1</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0014-4835
ispartof Experimental eye research, 2020-04, Vol.193, p.107981-107981, Article 107981
issn 0014-4835
1096-0007
language eng
recordid cdi_proquest_miscellaneous_2363090242
source Elsevier ScienceDirect Journals
subjects (Pro) renin/renin receptor
AT1 receptor
Hypertension
PEDF
Preeclampsia
Pregnancy
Retinopathy
VEGF
title Preeclampsia as predisposing factor for hypertensive retinopathy: Participation by the RAAS and angiogenic factors
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T12%3A17%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Preeclampsia%20as%20predisposing%20factor%20for%20hypertensive%20retinopathy:%20Participation%20by%20the%20RAAS%20and%20angiogenic%20factors&rft.jtitle=Experimental%20eye%20research&rft.au=Ram%C3%ADrez-Montero,%20Claudia&rft.date=2020-04&rft.volume=193&rft.spage=107981&rft.epage=107981&rft.pages=107981-107981&rft.artnum=107981&rft.issn=0014-4835&rft.eissn=1096-0007&rft_id=info:doi/10.1016/j.exer.2020.107981&rft_dat=%3Cproquest_cross%3E2363090242%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2363090242&rft_id=info:pmid/32088240&rft_els_id=S0014483519308474&rfr_iscdi=true