Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance

B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. Cardiac contractility, ROS, and NO generation, and protein expressio...

Full description

Saved in:
Bibliographic Details
Published in:Life sciences (1973) 2019-07, Vol.228, p.121-127
Main Authors: Mesquita, Thássio Ricardo Ribeiro, Miguel-dos-Santos, Rodrigo, Jesus, Itamar Couto Guedes de, de Almeida, Grace Kelly Melo, Fernandes, Valéria Alves, Gomes, Aline Alves Lara, Guatimosim, Silvia, Martins-Silva, Leonardo, Ferreira, Anderson José, Capettini, Luciano dos Santos Aggum, Pesquero, Jorge Luís, Lauton-Santos, Sandra
Format: Article
Language:English
Subjects:
Ablation
Adenosine triphosphatase
Ca2+-transporting ATPase
Calcium (reticular)
Calcium ions
Cardiac
Cardiac muscle
Cardiovascular diseases
Heart diseases
Kinin receptors
Muscle contraction
NAD(P)H oxidase
NADPH oxidase
Nitration
Nitric oxide
Oxidative stress
Peroxynitrite
Reactive oxygen species
Receptors
Sarcoplasmic reticulum
Tyrosine
Unbalance
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-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403
cites cdi_FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403
container_end_page 127
container_issue
container_start_page 121
container_title Life sciences (1973)
container_volume 228
creator Mesquita, Thássio Ricardo Ribeiro
Miguel-dos-Santos, Rodrigo
Jesus, Itamar Couto Guedes de
de Almeida, Grace Kelly Melo
Fernandes, Valéria Alves
Gomes, Aline Alves Lara
Guatimosim, Silvia
Martins-Silva, Leonardo
Ferreira, Anderson José
Capettini, Luciano dos Santos Aggum
Pesquero, Jorge Luís
Lauton-Santos, Sandra
description B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1−/−) and B2-kinin (B2−/−) knockout mice. Impaired contractility in B1−/− and B2−/− hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1−/− and B2−/− hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1−/− and B2−/− hearts. B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.
doi_str_mv 10.1016/j.lfs.2019.04.062
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2218303023</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0024320519303303</els_id><sourcerecordid>2218303023</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403</originalsourceid><addsrcrecordid>eNp9kDtPwzAUhS0EEuXxA9gisbAkXD8SN2JqES-pEgvMluMHdUntYieI_ntcysTAdJbvXJ37IXSBocKAm-tV1dtUEcBtBayChhygCZ7ytoSG4kM0ASCspATqY3SS0goA6prTCZKzrpeDC74ItpjjspBeF3NSvjvvfBGNMpshxFQoOSazi6idVIXeJjt69VMcljGMb8sM6_BVejfEkEIx-k720itzho6s7JM5_81T9Hp_93L7WC6eH55uZ4tSEaC05LijDLQB2gF0mFre2pazlssWtGWaGcIN1ZjUVDUaWyt52xhMp5ypqWVAT9HV_u4mho_RpEGsXVKmzyNMGJMgBE8pUCA0o5d_0FUYo8_rMsUYrgltWabwnlL5oRSNFZvo1jJuBQaxky5WIksXO-kCmMjSc-dm3zH5009nokjKmWxBu-xyEDq4f9rfPIaI0w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2244152394</pqid></control><display><type>article</type><title>Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance</title><source>ScienceDirect Freedom Collection</source><creator>Mesquita, Thássio Ricardo Ribeiro ; Miguel-dos-Santos, Rodrigo ; Jesus, Itamar Couto Guedes de ; de Almeida, Grace Kelly Melo ; Fernandes, Valéria Alves ; Gomes, Aline Alves Lara ; Guatimosim, Silvia ; Martins-Silva, Leonardo ; Ferreira, Anderson José ; Capettini, Luciano dos Santos Aggum ; Pesquero, Jorge Luís ; Lauton-Santos, Sandra</creator><creatorcontrib>Mesquita, Thássio Ricardo Ribeiro ; Miguel-dos-Santos, Rodrigo ; Jesus, Itamar Couto Guedes de ; de Almeida, Grace Kelly Melo ; Fernandes, Valéria Alves ; Gomes, Aline Alves Lara ; Guatimosim, Silvia ; Martins-Silva, Leonardo ; Ferreira, Anderson José ; Capettini, Luciano dos Santos Aggum ; Pesquero, Jorge Luís ; Lauton-Santos, Sandra</creatorcontrib><description>B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1−/−) and B2-kinin (B2−/−) knockout mice. Impaired contractility in B1−/− and B2−/− hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1−/− and B2−/− hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1−/− and B2−/− hearts. B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2019.04.062</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Ablation ; Adenosine triphosphatase ; Ca2+-transporting ATPase ; Calcium (reticular) ; Calcium ions ; Cardiac ; Cardiac muscle ; Cardiovascular diseases ; Heart diseases ; Kinin receptors ; Muscle contraction ; NAD(P)H oxidase ; NADPH oxidase ; Nitration ; Nitric oxide ; Oxidative stress ; Peroxynitrite ; Reactive oxygen species ; Receptors ; Sarcoplasmic reticulum ; Tyrosine ; Unbalance</subject><ispartof>Life sciences (1973), 2019-07, Vol.228, p.121-127</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright Elsevier BV Jul 1, 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403</citedby><cites>FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403</cites><orcidid>0000-0003-3524-4876 ; 0000-0002-6927-5745</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids></links><search><creatorcontrib>Mesquita, Thássio Ricardo Ribeiro</creatorcontrib><creatorcontrib>Miguel-dos-Santos, Rodrigo</creatorcontrib><creatorcontrib>Jesus, Itamar Couto Guedes de</creatorcontrib><creatorcontrib>de Almeida, Grace Kelly Melo</creatorcontrib><creatorcontrib>Fernandes, Valéria Alves</creatorcontrib><creatorcontrib>Gomes, Aline Alves Lara</creatorcontrib><creatorcontrib>Guatimosim, Silvia</creatorcontrib><creatorcontrib>Martins-Silva, Leonardo</creatorcontrib><creatorcontrib>Ferreira, Anderson José</creatorcontrib><creatorcontrib>Capettini, Luciano dos Santos Aggum</creatorcontrib><creatorcontrib>Pesquero, Jorge Luís</creatorcontrib><creatorcontrib>Lauton-Santos, Sandra</creatorcontrib><title>Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance</title><title>Life sciences (1973)</title><description>B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1−/−) and B2-kinin (B2−/−) knockout mice. Impaired contractility in B1−/− and B2−/− hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1−/− and B2−/− hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1−/− and B2−/− hearts. B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.</description><subject>Ablation</subject><subject>Adenosine triphosphatase</subject><subject>Ca2+-transporting ATPase</subject><subject>Calcium (reticular)</subject><subject>Calcium ions</subject><subject>Cardiac</subject><subject>Cardiac muscle</subject><subject>Cardiovascular diseases</subject><subject>Heart diseases</subject><subject>Kinin receptors</subject><subject>Muscle contraction</subject><subject>NAD(P)H oxidase</subject><subject>NADPH oxidase</subject><subject>Nitration</subject><subject>Nitric oxide</subject><subject>Oxidative stress</subject><subject>Peroxynitrite</subject><subject>Reactive oxygen species</subject><subject>Receptors</subject><subject>Sarcoplasmic reticulum</subject><subject>Tyrosine</subject><subject>Unbalance</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kDtPwzAUhS0EEuXxA9gisbAkXD8SN2JqES-pEgvMluMHdUntYieI_ntcysTAdJbvXJ37IXSBocKAm-tV1dtUEcBtBayChhygCZ7ytoSG4kM0ASCspATqY3SS0goA6prTCZKzrpeDC74ItpjjspBeF3NSvjvvfBGNMpshxFQoOSazi6idVIXeJjt69VMcljGMb8sM6_BVejfEkEIx-k720itzho6s7JM5_81T9Hp_93L7WC6eH55uZ4tSEaC05LijDLQB2gF0mFre2pazlssWtGWaGcIN1ZjUVDUaWyt52xhMp5ypqWVAT9HV_u4mho_RpEGsXVKmzyNMGJMgBE8pUCA0o5d_0FUYo8_rMsUYrgltWabwnlL5oRSNFZvo1jJuBQaxky5WIksXO-kCmMjSc-dm3zH5009nokjKmWxBu-xyEDq4f9rfPIaI0w</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Mesquita, Thássio Ricardo Ribeiro</creator><creator>Miguel-dos-Santos, Rodrigo</creator><creator>Jesus, Itamar Couto Guedes de</creator><creator>de Almeida, Grace Kelly Melo</creator><creator>Fernandes, Valéria Alves</creator><creator>Gomes, Aline Alves Lara</creator><creator>Guatimosim, Silvia</creator><creator>Martins-Silva, Leonardo</creator><creator>Ferreira, Anderson José</creator><creator>Capettini, Luciano dos Santos Aggum</creator><creator>Pesquero, Jorge Luís</creator><creator>Lauton-Santos, Sandra</creator><general>Elsevier Inc</general><general>Elsevier BV</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3524-4876</orcidid><orcidid>https://orcid.org/0000-0002-6927-5745</orcidid></search><sort><creationdate>20190701</creationdate><title>Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance</title><author>Mesquita, Thássio Ricardo Ribeiro ; Miguel-dos-Santos, Rodrigo ; Jesus, Itamar Couto Guedes de ; de Almeida, Grace Kelly Melo ; Fernandes, Valéria Alves ; Gomes, Aline Alves Lara ; Guatimosim, Silvia ; Martins-Silva, Leonardo ; Ferreira, Anderson José ; Capettini, Luciano dos Santos Aggum ; Pesquero, Jorge Luís ; Lauton-Santos, Sandra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Ablation</topic><topic>Adenosine triphosphatase</topic><topic>Ca2+-transporting ATPase</topic><topic>Calcium (reticular)</topic><topic>Calcium ions</topic><topic>Cardiac</topic><topic>Cardiac muscle</topic><topic>Cardiovascular diseases</topic><topic>Heart diseases</topic><topic>Kinin receptors</topic><topic>Muscle contraction</topic><topic>NAD(P)H oxidase</topic><topic>NADPH oxidase</topic><topic>Nitration</topic><topic>Nitric oxide</topic><topic>Oxidative stress</topic><topic>Peroxynitrite</topic><topic>Reactive oxygen species</topic><topic>Receptors</topic><topic>Sarcoplasmic reticulum</topic><topic>Tyrosine</topic><topic>Unbalance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mesquita, Thássio Ricardo Ribeiro</creatorcontrib><creatorcontrib>Miguel-dos-Santos, Rodrigo</creatorcontrib><creatorcontrib>Jesus, Itamar Couto Guedes de</creatorcontrib><creatorcontrib>de Almeida, Grace Kelly Melo</creatorcontrib><creatorcontrib>Fernandes, Valéria Alves</creatorcontrib><creatorcontrib>Gomes, Aline Alves Lara</creatorcontrib><creatorcontrib>Guatimosim, Silvia</creatorcontrib><creatorcontrib>Martins-Silva, Leonardo</creatorcontrib><creatorcontrib>Ferreira, Anderson José</creatorcontrib><creatorcontrib>Capettini, Luciano dos Santos Aggum</creatorcontrib><creatorcontrib>Pesquero, Jorge Luís</creatorcontrib><creatorcontrib>Lauton-Santos, Sandra</creatorcontrib><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mesquita, Thássio Ricardo Ribeiro</au><au>Miguel-dos-Santos, Rodrigo</au><au>Jesus, Itamar Couto Guedes de</au><au>de Almeida, Grace Kelly Melo</au><au>Fernandes, Valéria Alves</au><au>Gomes, Aline Alves Lara</au><au>Guatimosim, Silvia</au><au>Martins-Silva, Leonardo</au><au>Ferreira, Anderson José</au><au>Capettini, Luciano dos Santos Aggum</au><au>Pesquero, Jorge Luís</au><au>Lauton-Santos, Sandra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance</atitle><jtitle>Life sciences (1973)</jtitle><date>2019-07-01</date><risdate>2019</risdate><volume>228</volume><spage>121</spage><epage>127</epage><pages>121-127</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation. Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1−/−) and B2-kinin (B2−/−) knockout mice. Impaired contractility in B1−/− and B2−/− hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1−/− and B2−/− hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1−/− and B2−/− hearts. B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><doi>10.1016/j.lfs.2019.04.062</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-3524-4876</orcidid><orcidid>https://orcid.org/0000-0002-6927-5745</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0024-3205
ispartof Life sciences (1973), 2019-07, Vol.228, p.121-127
issn 0024-3205
1879-0631
language eng
recordid cdi_proquest_miscellaneous_2218303023
source ScienceDirect Freedom Collection
subjects Ablation
Adenosine triphosphatase
Ca2+-transporting ATPase
Calcium (reticular)
Calcium ions
Cardiac
Cardiac muscle
Cardiovascular diseases
Heart diseases
Kinin receptors
Muscle contraction
NAD(P)H oxidase
NADPH oxidase
Nitration
Nitric oxide
Oxidative stress
Peroxynitrite
Reactive oxygen species
Receptors
Sarcoplasmic reticulum
Tyrosine
Unbalance
title Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T14%3A45%3A39IST&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=Ablation%20of%20B1-%20and%20B2-kinin%20receptors%20causes%20cardiac%20dysfunction%20through%20redox-nitroso%20unbalance&rft.jtitle=Life%20sciences%20(1973)&rft.au=Mesquita,%20Th%C3%A1ssio%20Ricardo%20Ribeiro&rft.date=2019-07-01&rft.volume=228&rft.spage=121&rft.epage=127&rft.pages=121-127&rft.issn=0024-3205&rft.eissn=1879-0631&rft_id=info:doi/10.1016/j.lfs.2019.04.062&rft_dat=%3Cproquest_cross%3E2218303023%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c2033-71b340de03b00b13f79f97497a90df4d4e27e3d1253c6d1ffa796e13874c8f403%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2244152394&rft_id=info:pmid/&rfr_iscdi=true