High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism

Detalhes bibliográficos
Autor(a) principal: Morais, Rafael L. [UNIFESP]
Data de Publicação: 2017
Outros Autores: Hilzendeger, Aline M. [UNIFESP], Visniauskas, Bruna [UNIFESP], Todiras, Mihail, Alenina, Natalia, Mori, Marcelo A. [UNIFESP], Araujo, Ronaldo C. [UNIFESP], Nakaie, Clovis R. [UNIFESP], Chagas, Jair R. [UNIFESP], Carmona, Adriana K. [UNIFESP], Bader, Michael, Pesquero, Joao B. [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://dx.doi.org/10.1152/ajpheart.00485.2016
https://repositorio.unifesp.br/handle/11600/55035
Resumo: Obesity is assumed to be a major cause of human essential hypertension
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spelling High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanismaminopeptidase Ahypertensionobesityrenin-angiotensin-aldosterone systemob/ob miceObesity is assumed to be a major cause of human essential hypertensionhowever, the mechanisms responsible for weight-related increase in blood pressure (BP) are not fully understood. The prevalence of hypertension induced by obesity has grown over the years, and the role of the renin-angiotensin-aldosterone system (RAAS) in this process continues to be elucidated. In this scenario, the ob/ob mice are a genetic obesity model generally used for metabolic disorder studies. These mice are normotensive even though they present several metabolic conditions that predispose them to hypertension. Although the normotensive trait in these mice is associated with the poor activation of sympathetic nervous system by the lack of leptin, we demonstrated that ob/ob mice present massively increased aminopeptidase A (APA) activity in the circulation. APA enzyme metabolizes angiotensin (ANG) II into ANG III, a peptide associated with intrarenal angiotensin type 2 (AT(2)) receptor activation and induction of natriuresis. In these mice, we found increased ANG-III levels in the circulation, high AT(2) receptor expression in the kidney, and enhanced natriuresis. AT(2) receptor blocking and APA inhibition increased BP, suggesting the ANG III-AT(2) receptor axis as a complementary BP control mechanism. Circulating APA activity was significantly reduced by weight loss independently of leptin, indicating the role of fat tissue in APA production. Therefore, in this study we provide new data supporting the role of APA in BP control in ob/ob mouse strain. These findings improve our comprehension about obesity-related hypertension and suggest new tools for its treatment. NEW & NOTEWORTHY In this study, we reported an increased angiotensin III generation in the circulation of ob/ob mice caused by a high aminopeptidase A activity. These findings are associated with an increased natriuresis found in these mice and support the role of renin-angiotensin-aldosterone system as additional mechanism regulating blood pressure in this genetic obese strain.Univ Fed Sao Paulo, Dept Biofis, Campus Sao Paulo, Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Psicobiol, Campus Sao Paulo, Sao Paulo, BrazilMax Delbruck Ctr Mol Med, Berlin, GermanyCharite Univ Med Berlin, Berlin, GermanyGerman Ctr Cardiovasc Res, Berlin, GermanyUniv Lubeck, Inst Biol, Lubeck, GermanyUniv Fed Sao Paulo, Dept Biofis, Campus Sao Paulo, Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Psicobiol, Campus Sao Paulo, Sao Paulo, BrazilWeb of ScienceFundacao de Amparo a Pesquisa do Estado de Sao PauloConselho Nacional de Desenvolvimento Cientifico e TecnologicoCoordenacao de Aperfeicoamento de Pessoal de Nivel SuperiorAmer Physiological Soc2020-07-17T14:02:48Z2020-07-17T14:02:48Z2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionH437-H445http://dx.doi.org/10.1152/ajpheart.00485.2016American Journal Of Physiology-Heart And Circulatory Physiology. Bethesda, v. 312, n. 3, p. H437-H445, 2017.10.1152/ajpheart.00485.20160363-6135https://repositorio.unifesp.br/handle/11600/55035WOS:000397808500010engAmerican Journal Of Physiology-Heart And Circulatory PhysiologyBethesdainfo:eu-repo/semantics/openAccessMorais, Rafael L. [UNIFESP]Hilzendeger, Aline M. [UNIFESP]Visniauskas, Bruna [UNIFESP]Todiras, MihailAlenina, NataliaMori, Marcelo A. [UNIFESP]Araujo, Ronaldo C. [UNIFESP]Nakaie, Clovis R. [UNIFESP]Chagas, Jair R. [UNIFESP]Carmona, Adriana K. [UNIFESP]Bader, MichaelPesquero, Joao B. [UNIFESP]reponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2021-09-29T11:28:08Zoai:repositorio.unifesp.br/:11600/55035Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652021-09-29T11:28:08Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.none.fl_str_mv High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
title High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
spellingShingle High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
Morais, Rafael L. [UNIFESP]
aminopeptidase A
hypertension
obesity
renin-angiotensin-aldosterone system
ob/ob mice
title_short High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
title_full High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
title_fullStr High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
title_full_unstemmed High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
title_sort High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
author Morais, Rafael L. [UNIFESP]
author_facet Morais, Rafael L. [UNIFESP]
Hilzendeger, Aline M. [UNIFESP]
Visniauskas, Bruna [UNIFESP]
Todiras, Mihail
Alenina, Natalia
Mori, Marcelo A. [UNIFESP]
Araujo, Ronaldo C. [UNIFESP]
Nakaie, Clovis R. [UNIFESP]
Chagas, Jair R. [UNIFESP]
Carmona, Adriana K. [UNIFESP]
Bader, Michael
Pesquero, Joao B. [UNIFESP]
author_role author
author2 Hilzendeger, Aline M. [UNIFESP]
Visniauskas, Bruna [UNIFESP]
Todiras, Mihail
Alenina, Natalia
Mori, Marcelo A. [UNIFESP]
Araujo, Ronaldo C. [UNIFESP]
Nakaie, Clovis R. [UNIFESP]
Chagas, Jair R. [UNIFESP]
Carmona, Adriana K. [UNIFESP]
Bader, Michael
Pesquero, Joao B. [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Morais, Rafael L. [UNIFESP]
Hilzendeger, Aline M. [UNIFESP]
Visniauskas, Bruna [UNIFESP]
Todiras, Mihail
Alenina, Natalia
Mori, Marcelo A. [UNIFESP]
Araujo, Ronaldo C. [UNIFESP]
Nakaie, Clovis R. [UNIFESP]
Chagas, Jair R. [UNIFESP]
Carmona, Adriana K. [UNIFESP]
Bader, Michael
Pesquero, Joao B. [UNIFESP]
dc.subject.por.fl_str_mv aminopeptidase A
hypertension
obesity
renin-angiotensin-aldosterone system
ob/ob mice
topic aminopeptidase A
hypertension
obesity
renin-angiotensin-aldosterone system
ob/ob mice
description Obesity is assumed to be a major cause of human essential hypertension
publishDate 2017
dc.date.none.fl_str_mv 2017
2020-07-17T14:02:48Z
2020-07-17T14:02:48Z
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1152/ajpheart.00485.2016
American Journal Of Physiology-Heart And Circulatory Physiology. Bethesda, v. 312, n. 3, p. H437-H445, 2017.
10.1152/ajpheart.00485.2016
0363-6135
https://repositorio.unifesp.br/handle/11600/55035
WOS:000397808500010
url http://dx.doi.org/10.1152/ajpheart.00485.2016
https://repositorio.unifesp.br/handle/11600/55035
identifier_str_mv American Journal Of Physiology-Heart And Circulatory Physiology. Bethesda, v. 312, n. 3, p. H437-H445, 2017.
10.1152/ajpheart.00485.2016
0363-6135
WOS:000397808500010
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv American Journal Of Physiology-Heart And Circulatory Physiology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv H437-H445
dc.coverage.none.fl_str_mv Bethesda
dc.publisher.none.fl_str_mv Amer Physiological Soc
publisher.none.fl_str_mv Amer Physiological Soc
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv biblioteca.csp@unifesp.br
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