Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition

Autores
Giani, Jorge Fernando; Janjulia, Tea; Kamat, Nikhil; Seth, Dale M.; Blackwell, Wendell-Lamar B.; Shah, Kandarp H.; Shen, Xiao Z.; Fuchs, Sebastien; Delpire, Eric; Toblli, Jorge Eduardo; Bernstein, Kenneth E.; McDonough, Alicia A.; Gonzalez Villalobos, Romer A.
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The kidney is an important source of angiotensin-converting enzyme (ACE) in many species, including humans. However, the specific effects of local ACE on renal function and, by extension, BP control are not completely understood. We previously showed that mice lacking renal ACE, are resistant to the hypertension induced by angiotensin II infusion. Here, we examined the responses of these mice to the low-systemic angiotensin II hypertensive model of nitric oxide synthesis inhibition with L-NAME. In contrast to wild-type mice, mice without renal ACE did not develop hypertension, had lower renal angiotensin II levels, and enhanced natriuresis in response to L-NAME. During L-NAME treatment, the absence of renal ACE was associated with blunted GFR responses; greater reductions in abundance of proximal tubule Na+/H+ exchanger 3, Na+/Pi co-transporter 2, phosphorylated Na+/K+/Cl- cotransporter, and phosphorylated Na+/Cl- cotransporter; and greater reductions in abundance and processing of the γ isoform of the epithelial Na+ channel. In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition.
Fil: Giani, Jorge Fernando. Cedars Sinai Medical Center; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Janjulia, Tea. Cedars Sinai Medical Center; Estados Unidos
Fil: Kamat, Nikhil. University of Southern California; Estados Unidos
Fil: Seth, Dale M.. University of Tulane; Estados Unidos
Fil: Blackwell, Wendell-Lamar B.. Cedars Sinai Medical Center; Estados Unidos
Fil: Shah, Kandarp H.. Cedars Sinai Medical Center; Estados Unidos
Fil: Shen, Xiao Z.. Cedars Sinai Medical Center; Estados Unidos
Fil: Fuchs, Sebastien. Western University of Health Sciences; Estados Unidos
Fil: Delpire, Eric. Vanderbilt University; Estados Unidos
Fil: Toblli, Jorge Eduardo. Hospital Aleman; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Bernstein, Kenneth E.. Cedars Sinai Medical Center; Estados Unidos
Fil: McDonough, Alicia A.. University of Southern California; Estados Unidos
Fil: Gonzalez Villalobos, Romer A.. Cedars Sinai Medical Center; Estados Unidos
Materia
Angiotensin Ii
Ace
Inflammation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/37211
Acceder
id CONICETDig_df996f6ae5a68f45fa6cc4def28c4add
oai_identifier_str oai:ri.conicet.gov.ar:11336/37211
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibitionGiani, Jorge FernandoJanjulia, TeaKamat, NikhilSeth, Dale M.Blackwell, Wendell-Lamar B.Shah, Kandarp H.Shen, Xiao Z.Fuchs, SebastienDelpire, EricToblli, Jorge EduardoBernstein, Kenneth E.McDonough, Alicia A.Gonzalez Villalobos, Romer A.Angiotensin IiAceInflammationhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3The kidney is an important source of angiotensin-converting enzyme (ACE) in many species, including humans. However, the specific effects of local ACE on renal function and, by extension, BP control are not completely understood. We previously showed that mice lacking renal ACE, are resistant to the hypertension induced by angiotensin II infusion. Here, we examined the responses of these mice to the low-systemic angiotensin II hypertensive model of nitric oxide synthesis inhibition with L-NAME. In contrast to wild-type mice, mice without renal ACE did not develop hypertension, had lower renal angiotensin II levels, and enhanced natriuresis in response to L-NAME. During L-NAME treatment, the absence of renal ACE was associated with blunted GFR responses; greater reductions in abundance of proximal tubule Na+/H+ exchanger 3, Na+/Pi co-transporter 2, phosphorylated Na+/K+/Cl- cotransporter, and phosphorylated Na+/Cl- cotransporter; and greater reductions in abundance and processing of the γ isoform of the epithelial Na+ channel. In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition.Fil: Giani, Jorge Fernando. Cedars Sinai Medical Center; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Janjulia, Tea. Cedars Sinai Medical Center; Estados UnidosFil: Kamat, Nikhil. University of Southern California; Estados UnidosFil: Seth, Dale M.. University of Tulane; Estados UnidosFil: Blackwell, Wendell-Lamar B.. Cedars Sinai Medical Center; Estados UnidosFil: Shah, Kandarp H.. Cedars Sinai Medical Center; Estados UnidosFil: Shen, Xiao Z.. Cedars Sinai Medical Center; Estados UnidosFil: Fuchs, Sebastien. Western University of Health Sciences; Estados UnidosFil: Delpire, Eric. Vanderbilt University; Estados UnidosFil: Toblli, Jorge Eduardo. Hospital Aleman; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bernstein, Kenneth E.. Cedars Sinai Medical Center; Estados UnidosFil: McDonough, Alicia A.. University of Southern California; Estados UnidosFil: Gonzalez Villalobos, Romer A.. Cedars Sinai Medical Center; Estados UnidosAmer Soc Nephrology2014-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/37211Giani, Jorge Fernando; Janjulia, Tea; Kamat, Nikhil; Seth, Dale M.; Blackwell, Wendell-Lamar B.; et al.; Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition; Amer Soc Nephrology; Journal Of The American Society Of Nephrology; 25; 12; 12-2014; 2752-27631046-6673CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1681/ASN.2013091030info:eu-repo/semantics/altIdentifier/url/http://jasn.asnjournals.org/content/25/12/2752info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:05:40Zoai:ri.conicet.gov.ar:11336/37211instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:05:40.998CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
title Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
spellingShingle Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
Giani, Jorge Fernando
Angiotensin Ii
Ace
Inflammation
title_short Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
title_full Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
title_fullStr Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
title_full_unstemmed Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
title_sort Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition
dc.creator.none.fl_str_mv Giani, Jorge Fernando
Janjulia, Tea
Kamat, Nikhil
Seth, Dale M.
Blackwell, Wendell-Lamar B.
Shah, Kandarp H.
Shen, Xiao Z.
Fuchs, Sebastien
Delpire, Eric
Toblli, Jorge Eduardo
Bernstein, Kenneth E.
McDonough, Alicia A.
Gonzalez Villalobos, Romer A.
author Giani, Jorge Fernando
author_facet Giani, Jorge Fernando
Janjulia, Tea
Kamat, Nikhil
Seth, Dale M.
Blackwell, Wendell-Lamar B.
Shah, Kandarp H.
Shen, Xiao Z.
Fuchs, Sebastien
Delpire, Eric
Toblli, Jorge Eduardo
Bernstein, Kenneth E.
McDonough, Alicia A.
Gonzalez Villalobos, Romer A.
author_role author
author2 Janjulia, Tea
Kamat, Nikhil
Seth, Dale M.
Blackwell, Wendell-Lamar B.
Shah, Kandarp H.
Shen, Xiao Z.
Fuchs, Sebastien
Delpire, Eric
Toblli, Jorge Eduardo
Bernstein, Kenneth E.
McDonough, Alicia A.
Gonzalez Villalobos, Romer A.
author2_role author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Angiotensin Ii
Ace
Inflammation
topic Angiotensin Ii
Ace
Inflammation
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The kidney is an important source of angiotensin-converting enzyme (ACE) in many species, including humans. However, the specific effects of local ACE on renal function and, by extension, BP control are not completely understood. We previously showed that mice lacking renal ACE, are resistant to the hypertension induced by angiotensin II infusion. Here, we examined the responses of these mice to the low-systemic angiotensin II hypertensive model of nitric oxide synthesis inhibition with L-NAME. In contrast to wild-type mice, mice without renal ACE did not develop hypertension, had lower renal angiotensin II levels, and enhanced natriuresis in response to L-NAME. During L-NAME treatment, the absence of renal ACE was associated with blunted GFR responses; greater reductions in abundance of proximal tubule Na+/H+ exchanger 3, Na+/Pi co-transporter 2, phosphorylated Na+/K+/Cl- cotransporter, and phosphorylated Na+/Cl- cotransporter; and greater reductions in abundance and processing of the γ isoform of the epithelial Na+ channel. In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition.
Fil: Giani, Jorge Fernando. Cedars Sinai Medical Center; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Janjulia, Tea. Cedars Sinai Medical Center; Estados Unidos
Fil: Kamat, Nikhil. University of Southern California; Estados Unidos
Fil: Seth, Dale M.. University of Tulane; Estados Unidos
Fil: Blackwell, Wendell-Lamar B.. Cedars Sinai Medical Center; Estados Unidos
Fil: Shah, Kandarp H.. Cedars Sinai Medical Center; Estados Unidos
Fil: Shen, Xiao Z.. Cedars Sinai Medical Center; Estados Unidos
Fil: Fuchs, Sebastien. Western University of Health Sciences; Estados Unidos
Fil: Delpire, Eric. Vanderbilt University; Estados Unidos
Fil: Toblli, Jorge Eduardo. Hospital Aleman; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Bernstein, Kenneth E.. Cedars Sinai Medical Center; Estados Unidos
Fil: McDonough, Alicia A.. University of Southern California; Estados Unidos
Fil: Gonzalez Villalobos, Romer A.. Cedars Sinai Medical Center; Estados Unidos
description The kidney is an important source of angiotensin-converting enzyme (ACE) in many species, including humans. However, the specific effects of local ACE on renal function and, by extension, BP control are not completely understood. We previously showed that mice lacking renal ACE, are resistant to the hypertension induced by angiotensin II infusion. Here, we examined the responses of these mice to the low-systemic angiotensin II hypertensive model of nitric oxide synthesis inhibition with L-NAME. In contrast to wild-type mice, mice without renal ACE did not develop hypertension, had lower renal angiotensin II levels, and enhanced natriuresis in response to L-NAME. During L-NAME treatment, the absence of renal ACE was associated with blunted GFR responses; greater reductions in abundance of proximal tubule Na+/H+ exchanger 3, Na+/Pi co-transporter 2, phosphorylated Na+/K+/Cl- cotransporter, and phosphorylated Na+/Cl- cotransporter; and greater reductions in abundance and processing of the γ isoform of the epithelial Na+ channel. In summary, the presence of ACE in renal tissue facilitates angiotensin II accumulation, GFR reductions, and changes in the expression levels and post-translational modification of sodium transporters that are obligatory for sodium retention and hypertension in response to nitric oxide synthesis inhibition.
publishDate 2014
dc.date.none.fl_str_mv 2014-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/37211
Giani, Jorge Fernando; Janjulia, Tea; Kamat, Nikhil; Seth, Dale M.; Blackwell, Wendell-Lamar B.; et al.; Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition; Amer Soc Nephrology; Journal Of The American Society Of Nephrology; 25; 12; 12-2014; 2752-2763
1046-6673
CONICET Digital
CONICET
url http://hdl.handle.net/11336/37211
identifier_str_mv Giani, Jorge Fernando; Janjulia, Tea; Kamat, Nikhil; Seth, Dale M.; Blackwell, Wendell-Lamar B.; et al.; Renal angiotensin-converting enzyme is essential for the hypertension induced by nitric oxide synthesis inhibition; Amer Soc Nephrology; Journal Of The American Society Of Nephrology; 25; 12; 12-2014; 2752-2763
1046-6673
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1681/ASN.2013091030
info:eu-repo/semantics/altIdentifier/url/http://jasn.asnjournals.org/content/25/12/2752
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Amer Soc Nephrology
publisher.none.fl_str_mv Amer Soc Nephrology
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269923093512192
score 13.13397

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