Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats

Autores
Della Penna, Silvana; Cao, Gabriel Fernando; Kouyoumdzian, Nicolás Martín; Sarati, Lorena Ivonne; Fellet, Andrea L.; Balaszczuk, Ana María; Choi, Marcelo Roberto; Zotta, Elsa; Gorzalczany, Susana Beatriz; Pandolfo, Marcela; Toblli, Jorge Eduardo; Roson, Maria Ines; Fernandez, Belisario Enrique
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Groups of anesthetized male Sprague-Dawley rats were infused with isotonic saline solution (control) or with hypertonic saline solution (Na group, 1 M NaCl), either alone or with losartan (10 mg kg(-1)) or tempol (0.5 mg min(-1) kg(-1)) during 2 h. Renal function parameters were measured. Groups of unanesthetized animals were injected intraperitoneally with hypertonic saline solution, with or without free access to water intake, Na+W, and Na-W, respectively. The expression of AQP-1, AQP-2, Ang II, eNOS, and NF-kB were evaluated in the kidney by Western blot and immunohistochemistry. AQP-2 distribution was assessed by immunofluorescence. Na group showed increased natriuresis and diuresis, and Ang II and NF-kB expression, but decreased eNOS expression. Losartan or tempol enhanced further the diuresis, and AQP-2 and eNOS expression, as well as decreased Ang II and NF-kB expression. Confocal immunofluorescence imaging revealed labeling of AQP-2 in the apical plasma membrane with less labeling in the intracellular vesicles than the apical membrane in kidney medullary collecting duct principal cells both in C and Na groups. Importantly, our data also show that losartan and tempol induces a predominantly accumulation of AQP-2 in intracellular vesicles. In unanesthetized rats, Na+W group presented increased diuresis, natriuresis, and AQP-2 expression (112 ± 25 vs 64 ± 16; *p < 0.05). Water deprivation increased plasma sodium and diuresis but decreased AQP-2 (46 ± 22 vs 112 ± 25; §p < 0.05) and eNOS expression in the kidney. This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression.
Fil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Cao, Gabriel Fernando. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Sarati, Lorena. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Fellet, Andrea L.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Balaszczuk, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Choi, Marcelo Roberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Toblli, Jorge Eduardo. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Fernandez, Belisario Enrique. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
Angiotensin Ii
Oxidative Stress
Aquaporin
Hipernatremic Rats
Sodium Overload
Kidney
Losartan
Tempol
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:11336/30542

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oai_identifier_str oai:ri.conicet.gov.ar:11336/30542
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic ratsDella Penna, SilvanaCao, Gabriel FernandoKouyoumdzian, Nicolás MartínSarati, Lorena IvonneFellet, Andrea L.Balaszczuk, Ana MaríaChoi, Marcelo RobertoZotta, ElsaGorzalczany, Susana BeatrizPandolfo, MarcelaToblli, Jorge EduardoRoson, Maria InesFernandez, Belisario EnriqueAngiotensin IiOxidative StressAquaporinHipernatremic RatsSodium OverloadKidneyLosartanTempolhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Groups of anesthetized male Sprague-Dawley rats were infused with isotonic saline solution (control) or with hypertonic saline solution (Na group, 1 M NaCl), either alone or with losartan (10 mg kg(-1)) or tempol (0.5 mg min(-1) kg(-1)) during 2 h. Renal function parameters were measured. Groups of unanesthetized animals were injected intraperitoneally with hypertonic saline solution, with or without free access to water intake, Na+W, and Na-W, respectively. The expression of AQP-1, AQP-2, Ang II, eNOS, and NF-kB were evaluated in the kidney by Western blot and immunohistochemistry. AQP-2 distribution was assessed by immunofluorescence. Na group showed increased natriuresis and diuresis, and Ang II and NF-kB expression, but decreased eNOS expression. Losartan or tempol enhanced further the diuresis, and AQP-2 and eNOS expression, as well as decreased Ang II and NF-kB expression. Confocal immunofluorescence imaging revealed labeling of AQP-2 in the apical plasma membrane with less labeling in the intracellular vesicles than the apical membrane in kidney medullary collecting duct principal cells both in C and Na groups. Importantly, our data also show that losartan and tempol induces a predominantly accumulation of AQP-2 in intracellular vesicles. In unanesthetized rats, Na+W group presented increased diuresis, natriuresis, and AQP-2 expression (112 ± 25 vs 64 ± 16; *p < 0.05). Water deprivation increased plasma sodium and diuresis but decreased AQP-2 (46 ± 22 vs 112 ± 25; §p < 0.05) and eNOS expression in the kidney. This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression.Fil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; ArgentinaFil: Cao, Gabriel Fernando. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Sarati, Lorena. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Fellet, Andrea L.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Balaszczuk, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Choi, Marcelo Roberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Toblli, Jorge Eduardo. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fernandez, Belisario Enrique. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaSpringer2014-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/30542Della Penna, Silvana; Cao, Gabriel Fernando; Kouyoumdzian, Nicolás Martín; Sarati, Lorena Ivonne; Fellet, Andrea L.; et al.; Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats; Springer; Journal of Physiology and Biochemistry; 70; 2; 3-2014; 465-4781138-75481877-8755CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs13105-014-0324-5info:eu-repo/semantics/altIdentifier/doi/10.1007/s13105-014-0324-5info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:43Zoai:ri.conicet.gov.ar:11336/30542instacron: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 09:51:44.012CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
title Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
spellingShingle Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
Della Penna, Silvana
Angiotensin Ii
Oxidative Stress
Aquaporin
Hipernatremic Rats
Sodium Overload
Kidney
Losartan
Tempol
title_short Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
title_full Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
title_fullStr Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
title_full_unstemmed Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
title_sort Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats
dc.creator.none.fl_str_mv Della Penna, Silvana
Cao, Gabriel Fernando
Kouyoumdzian, Nicolás Martín
Sarati, Lorena Ivonne
Fellet, Andrea L.
Balaszczuk, Ana María
Choi, Marcelo Roberto
Zotta, Elsa
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Toblli, Jorge Eduardo
Roson, Maria Ines
Fernandez, Belisario Enrique
author Della Penna, Silvana
author_facet Della Penna, Silvana
Cao, Gabriel Fernando
Kouyoumdzian, Nicolás Martín
Sarati, Lorena Ivonne
Fellet, Andrea L.
Balaszczuk, Ana María
Choi, Marcelo Roberto
Zotta, Elsa
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Toblli, Jorge Eduardo
Roson, Maria Ines
Fernandez, Belisario Enrique
author_role author
author2 Cao, Gabriel Fernando
Kouyoumdzian, Nicolás Martín
Sarati, Lorena Ivonne
Fellet, Andrea L.
Balaszczuk, Ana María
Choi, Marcelo Roberto
Zotta, Elsa
Gorzalczany, Susana Beatriz
Pandolfo, Marcela
Toblli, Jorge Eduardo
Roson, Maria Ines
Fernandez, Belisario Enrique
author2_role author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Angiotensin Ii
Oxidative Stress
Aquaporin
Hipernatremic Rats
Sodium Overload
Kidney
Losartan
Tempol
topic Angiotensin Ii
Oxidative Stress
Aquaporin
Hipernatremic Rats
Sodium Overload
Kidney
Losartan
Tempol
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 aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Groups of anesthetized male Sprague-Dawley rats were infused with isotonic saline solution (control) or with hypertonic saline solution (Na group, 1 M NaCl), either alone or with losartan (10 mg kg(-1)) or tempol (0.5 mg min(-1) kg(-1)) during 2 h. Renal function parameters were measured. Groups of unanesthetized animals were injected intraperitoneally with hypertonic saline solution, with or without free access to water intake, Na+W, and Na-W, respectively. The expression of AQP-1, AQP-2, Ang II, eNOS, and NF-kB were evaluated in the kidney by Western blot and immunohistochemistry. AQP-2 distribution was assessed by immunofluorescence. Na group showed increased natriuresis and diuresis, and Ang II and NF-kB expression, but decreased eNOS expression. Losartan or tempol enhanced further the diuresis, and AQP-2 and eNOS expression, as well as decreased Ang II and NF-kB expression. Confocal immunofluorescence imaging revealed labeling of AQP-2 in the apical plasma membrane with less labeling in the intracellular vesicles than the apical membrane in kidney medullary collecting duct principal cells both in C and Na groups. Importantly, our data also show that losartan and tempol induces a predominantly accumulation of AQP-2 in intracellular vesicles. In unanesthetized rats, Na+W group presented increased diuresis, natriuresis, and AQP-2 expression (112 ± 25 vs 64 ± 16; *p < 0.05). Water deprivation increased plasma sodium and diuresis but decreased AQP-2 (46 ± 22 vs 112 ± 25; §p < 0.05) and eNOS expression in the kidney. This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression.
Fil: Della Penna, Silvana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Fisiopatología; Argentina
Fil: Cao, Gabriel Fernando. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Kouyoumdzian, Nicolás Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Sarati, Lorena. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Fellet, Andrea L.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Balaszczuk, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Choi, Marcelo Roberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Zotta, Elsa. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Gorzalczany, Susana Beatriz. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Pandolfo, Marcela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Toblli, Jorge Eduardo. Hospital Alemán. Laboratorio de Medicina Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Roson, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Fernandez, Belisario Enrique. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description The aim of this study was to assess whether endogenous Ang II and oxidative stress produced by acute hypertonic sodium overload may regulate the expression of aquaporin-1 (AQP-1) and aquaporin-2 (AQP-2) in the kidney. Groups of anesthetized male Sprague-Dawley rats were infused with isotonic saline solution (control) or with hypertonic saline solution (Na group, 1 M NaCl), either alone or with losartan (10 mg kg(-1)) or tempol (0.5 mg min(-1) kg(-1)) during 2 h. Renal function parameters were measured. Groups of unanesthetized animals were injected intraperitoneally with hypertonic saline solution, with or without free access to water intake, Na+W, and Na-W, respectively. The expression of AQP-1, AQP-2, Ang II, eNOS, and NF-kB were evaluated in the kidney by Western blot and immunohistochemistry. AQP-2 distribution was assessed by immunofluorescence. Na group showed increased natriuresis and diuresis, and Ang II and NF-kB expression, but decreased eNOS expression. Losartan or tempol enhanced further the diuresis, and AQP-2 and eNOS expression, as well as decreased Ang II and NF-kB expression. Confocal immunofluorescence imaging revealed labeling of AQP-2 in the apical plasma membrane with less labeling in the intracellular vesicles than the apical membrane in kidney medullary collecting duct principal cells both in C and Na groups. Importantly, our data also show that losartan and tempol induces a predominantly accumulation of AQP-2 in intracellular vesicles. In unanesthetized rats, Na+W group presented increased diuresis, natriuresis, and AQP-2 expression (112 ± 25 vs 64 ± 16; *p < 0.05). Water deprivation increased plasma sodium and diuresis but decreased AQP-2 (46 ± 22 vs 112 ± 25; §p < 0.05) and eNOS expression in the kidney. This study is a novel demonstration that renal endogenous Ang II-oxidative stress, induced in vivo in hypernatremic rats by an acute sodium overload, regulates AQP-2 expression.
publishDate 2014
dc.date.none.fl_str_mv 2014-03
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/11336/30542
Della Penna, Silvana; Cao, Gabriel Fernando; Kouyoumdzian, Nicolás Martín; Sarati, Lorena Ivonne; Fellet, Andrea L.; et al.; Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats; Springer; Journal of Physiology and Biochemistry; 70; 2; 3-2014; 465-478
1138-7548
1877-8755
CONICET Digital
CONICET
url http://hdl.handle.net/11336/30542
identifier_str_mv Della Penna, Silvana; Cao, Gabriel Fernando; Kouyoumdzian, Nicolás Martín; Sarati, Lorena Ivonne; Fellet, Andrea L.; et al.; Role of angiotensin II and oxidative stress on renal aquaporins expression in hypernatremic rats; Springer; Journal of Physiology and Biochemistry; 70; 2; 3-2014; 465-478
1138-7548
1877-8755
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs13105-014-0324-5
info:eu-repo/semantics/altIdentifier/doi/10.1007/s13105-014-0324-5
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
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dc.publisher.none.fl_str_mv Springer
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