High aminopeptidase A activity contributes to blood pressure control in ob/ob mice by AT(2) receptor-dependent mechanism
Autor(a) principal: | |
---|---|
Data de Publicação: | 2017 |
Outros Autores: | , , , , , , , , , , |
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 |
id |
UFSP_579ce26450c9f268a91fab13efe46871 |
---|---|
oai_identifier_str |
oai:repositorio.unifesp.br/:11600/55035 |
network_acronym_str |
UFSP |
network_name_str |
Repositório Institucional da UNIFESP |
repository_id_str |
3465 |
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 |
_version_ |
1814268363764924416 |