Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats

Autores
Mayer, Marcos Alejandro; Höcht, Christian; Giani, Jorge Fernando; Muñoz, Marina Cecilia; Carranza, A.; Taira, Carlos Alberto; Dominici, Fernando Pablo; Puyó, Ana María; Fernández, B. E.
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The aim of the present study was to determine if insulin is able to modulate the pressor response to intracerebroventricularly administered angiotensin II in insulin resistant fructose overloaded rats. Male Sprague-Dawley rats were divided into two groups: 1) Control group (C) with tap water to drink for 6 weeks (n = 36); and 2) fructose treated (F), with fructose solution (10% w/v) to drink for 6 weeks (n = 36). On the day of the experiment, anesthetized male C and F rats were intracerebroventricularly infused with insulin (12 mU/h, n = 15) or Ringer's solution as vehicle (n = 15) for 2 h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n = 10) or vehicle (n = 5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In a subset of C (n = 10) and F (n = 20) animals, PD98059 (p44/42 MAPK inhibitor) or vehicle was administered intracerebroventricularly at a flow rate of 5 μl/min for 1 min. Ten minutes later, insulin (12 mU/h, n = 5 for each group) or vehicle (Ringer's solution, only in the F group, n = 5) was perfused for 2 h at a flow rate of 4 μl/h, and cardiovascular parameters were measured every 15 min. Immediately, changes in MAP and HR in response to a subpressor dose of Ang II (5 pmol/2 μl) were evaluated for 10 min (n = 5 for each group). In other subset of animals (n = 6 for each group), AT1 and AT2 hypothalamic receptor levels were measured by Western blotting. Intracerebroventricular insulin pre-treatment increased the pressor response to angiotensin II in C rats. In F rats (with or without insulin pretreatment), the pressor response to angiotensin II was higher than that in vehicle pre-treated C animals, but similar to that observed in C after insulin infusion. In C rats phospho-ERK 1/2 hypothalamic levels significantly increased after angiotensin II injection in insulin pretreated animals compared to vehicle pre-treated rats, suggesting that MAPK activation might be involved in insulin potentiation of blood pressure response to angiotensin II in the brain. Phospho-ERK 1/2 hypothalamic levels were significantly increased in vehicle treated F rats compared to C, suggesting that basal MAPK activation might play a role in the enhanced response to angiotensin II observed in these animals. Finally, in F rats, either after vehicle or insulin infusion, angiotensin II injection was associated with a similar increase in phospho-ERK 1/2 hypothalamic levels, comparable to that observed after angiotensin II injection in insulin pre-treated C animals. ERK 1/2 blockade significantly reduced MAP in F rats compared to C. Moreover, ERK 1/2 inhibition completely abolished the Ang II pressor response in F rats and in insulin pre-treated C animals. All these findings suggest that insulin–angiotensin II interaction at hypothalamic level might be involved in the increase in blood pressure observed in the insulin resistant state.
Fil: Mayer, Marcos Alejandro. Fundación Centro de Salud e Investigaciones Médicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Giani, Jorge Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina
Fil: Muñoz, Marina Cecilia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Carranza, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Taira, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Dominici, Fernando Pablo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Puyó, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Fernández, B. E.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Materia
Hypertension
Fructose
Angiotensin
Insulin
Hypothalamus
Blood Pressure
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:11336/17890

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network_name_str CONICET Digital (CONICET)
spelling Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded ratsMayer, Marcos AlejandroHöcht, ChristianGiani, Jorge FernandoMuñoz, Marina CeciliaCarranza, A.Taira, Carlos AlbertoDominici, Fernando PabloPuyó, Ana MaríaFernández, B. E.HypertensionFructoseAngiotensinInsulinHypothalamusBlood Pressurehttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3The aim of the present study was to determine if insulin is able to modulate the pressor response to intracerebroventricularly administered angiotensin II in insulin resistant fructose overloaded rats. Male Sprague-Dawley rats were divided into two groups: 1) Control group (C) with tap water to drink for 6 weeks (n = 36); and 2) fructose treated (F), with fructose solution (10% w/v) to drink for 6 weeks (n = 36). On the day of the experiment, anesthetized male C and F rats were intracerebroventricularly infused with insulin (12 mU/h, n = 15) or Ringer's solution as vehicle (n = 15) for 2 h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n = 10) or vehicle (n = 5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In a subset of C (n = 10) and F (n = 20) animals, PD98059 (p44/42 MAPK inhibitor) or vehicle was administered intracerebroventricularly at a flow rate of 5 μl/min for 1 min. Ten minutes later, insulin (12 mU/h, n = 5 for each group) or vehicle (Ringer's solution, only in the F group, n = 5) was perfused for 2 h at a flow rate of 4 μl/h, and cardiovascular parameters were measured every 15 min. Immediately, changes in MAP and HR in response to a subpressor dose of Ang II (5 pmol/2 μl) were evaluated for 10 min (n = 5 for each group). In other subset of animals (n = 6 for each group), AT1 and AT2 hypothalamic receptor levels were measured by Western blotting. Intracerebroventricular insulin pre-treatment increased the pressor response to angiotensin II in C rats. In F rats (with or without insulin pretreatment), the pressor response to angiotensin II was higher than that in vehicle pre-treated C animals, but similar to that observed in C after insulin infusion. In C rats phospho-ERK 1/2 hypothalamic levels significantly increased after angiotensin II injection in insulin pretreated animals compared to vehicle pre-treated rats, suggesting that MAPK activation might be involved in insulin potentiation of blood pressure response to angiotensin II in the brain. Phospho-ERK 1/2 hypothalamic levels were significantly increased in vehicle treated F rats compared to C, suggesting that basal MAPK activation might play a role in the enhanced response to angiotensin II observed in these animals. Finally, in F rats, either after vehicle or insulin infusion, angiotensin II injection was associated with a similar increase in phospho-ERK 1/2 hypothalamic levels, comparable to that observed after angiotensin II injection in insulin pre-treated C animals. ERK 1/2 blockade significantly reduced MAP in F rats compared to C. Moreover, ERK 1/2 inhibition completely abolished the Ang II pressor response in F rats and in insulin pre-treated C animals. All these findings suggest that insulin–angiotensin II interaction at hypothalamic level might be involved in the increase in blood pressure observed in the insulin resistant state.Fil: Mayer, Marcos Alejandro. Fundación Centro de Salud e Investigaciones Médicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Giani, Jorge Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; ArgentinaFil: Muñoz, Marina Cecilia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Carranza, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Taira, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; ArgentinaFil: Dominici, Fernando Pablo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Puyó, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaFil: Fernández, B. E.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; ArgentinaElsevier Science2013-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/17890Mayer, Marcos Alejandro; Höcht, Christian; Giani, Jorge Fernando; Muñoz, Marina Cecilia; Carranza, A.; et al.; Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats; Elsevier Science; Regulatory Peptides; 185; 8-2013; 37-430167-0115enginfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0167011513000876info:eu-repo/semantics/altIdentifier/doi/10.1016/j.regpep.2013.06.001info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:53:06Zoai:ri.conicet.gov.ar:11336/17890instacron: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 09:53:07.27CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
title Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
spellingShingle Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
Mayer, Marcos Alejandro
Hypertension
Fructose
Angiotensin
Insulin
Hypothalamus
Blood Pressure
title_short Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
title_full Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
title_fullStr Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
title_full_unstemmed Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
title_sort Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats
dc.creator.none.fl_str_mv Mayer, Marcos Alejandro
Höcht, Christian
Giani, Jorge Fernando
Muñoz, Marina Cecilia
Carranza, A.
Taira, Carlos Alberto
Dominici, Fernando Pablo
Puyó, Ana María
Fernández, B. E.
author Mayer, Marcos Alejandro
author_facet Mayer, Marcos Alejandro
Höcht, Christian
Giani, Jorge Fernando
Muñoz, Marina Cecilia
Carranza, A.
Taira, Carlos Alberto
Dominici, Fernando Pablo
Puyó, Ana María
Fernández, B. E.
author_role author
author2 Höcht, Christian
Giani, Jorge Fernando
Muñoz, Marina Cecilia
Carranza, A.
Taira, Carlos Alberto
Dominici, Fernando Pablo
Puyó, Ana María
Fernández, B. E.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Hypertension
Fructose
Angiotensin
Insulin
Hypothalamus
Blood Pressure
topic Hypertension
Fructose
Angiotensin
Insulin
Hypothalamus
Blood Pressure
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.5
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The aim of the present study was to determine if insulin is able to modulate the pressor response to intracerebroventricularly administered angiotensin II in insulin resistant fructose overloaded rats. Male Sprague-Dawley rats were divided into two groups: 1) Control group (C) with tap water to drink for 6 weeks (n = 36); and 2) fructose treated (F), with fructose solution (10% w/v) to drink for 6 weeks (n = 36). On the day of the experiment, anesthetized male C and F rats were intracerebroventricularly infused with insulin (12 mU/h, n = 15) or Ringer's solution as vehicle (n = 15) for 2 h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n = 10) or vehicle (n = 5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In a subset of C (n = 10) and F (n = 20) animals, PD98059 (p44/42 MAPK inhibitor) or vehicle was administered intracerebroventricularly at a flow rate of 5 μl/min for 1 min. Ten minutes later, insulin (12 mU/h, n = 5 for each group) or vehicle (Ringer's solution, only in the F group, n = 5) was perfused for 2 h at a flow rate of 4 μl/h, and cardiovascular parameters were measured every 15 min. Immediately, changes in MAP and HR in response to a subpressor dose of Ang II (5 pmol/2 μl) were evaluated for 10 min (n = 5 for each group). In other subset of animals (n = 6 for each group), AT1 and AT2 hypothalamic receptor levels were measured by Western blotting. Intracerebroventricular insulin pre-treatment increased the pressor response to angiotensin II in C rats. In F rats (with or without insulin pretreatment), the pressor response to angiotensin II was higher than that in vehicle pre-treated C animals, but similar to that observed in C after insulin infusion. In C rats phospho-ERK 1/2 hypothalamic levels significantly increased after angiotensin II injection in insulin pretreated animals compared to vehicle pre-treated rats, suggesting that MAPK activation might be involved in insulin potentiation of blood pressure response to angiotensin II in the brain. Phospho-ERK 1/2 hypothalamic levels were significantly increased in vehicle treated F rats compared to C, suggesting that basal MAPK activation might play a role in the enhanced response to angiotensin II observed in these animals. Finally, in F rats, either after vehicle or insulin infusion, angiotensin II injection was associated with a similar increase in phospho-ERK 1/2 hypothalamic levels, comparable to that observed after angiotensin II injection in insulin pre-treated C animals. ERK 1/2 blockade significantly reduced MAP in F rats compared to C. Moreover, ERK 1/2 inhibition completely abolished the Ang II pressor response in F rats and in insulin pre-treated C animals. All these findings suggest that insulin–angiotensin II interaction at hypothalamic level might be involved in the increase in blood pressure observed in the insulin resistant state.
Fil: Mayer, Marcos Alejandro. Fundación Centro de Salud e Investigaciones Médicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Höcht, Christian. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Giani, Jorge Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina
Fil: Muñoz, Marina Cecilia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Carranza, A.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Taira, Carlos Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología; Argentina
Fil: Dominici, Fernando Pablo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Fil: Puyó, Ana María. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
Fil: Fernández, B. E.. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina
description The aim of the present study was to determine if insulin is able to modulate the pressor response to intracerebroventricularly administered angiotensin II in insulin resistant fructose overloaded rats. Male Sprague-Dawley rats were divided into two groups: 1) Control group (C) with tap water to drink for 6 weeks (n = 36); and 2) fructose treated (F), with fructose solution (10% w/v) to drink for 6 weeks (n = 36). On the day of the experiment, anesthetized male C and F rats were intracerebroventricularly infused with insulin (12 mU/h, n = 15) or Ringer's solution as vehicle (n = 15) for 2 h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n = 10) or vehicle (n = 5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In a subset of C (n = 10) and F (n = 20) animals, PD98059 (p44/42 MAPK inhibitor) or vehicle was administered intracerebroventricularly at a flow rate of 5 μl/min for 1 min. Ten minutes later, insulin (12 mU/h, n = 5 for each group) or vehicle (Ringer's solution, only in the F group, n = 5) was perfused for 2 h at a flow rate of 4 μl/h, and cardiovascular parameters were measured every 15 min. Immediately, changes in MAP and HR in response to a subpressor dose of Ang II (5 pmol/2 μl) were evaluated for 10 min (n = 5 for each group). In other subset of animals (n = 6 for each group), AT1 and AT2 hypothalamic receptor levels were measured by Western blotting. Intracerebroventricular insulin pre-treatment increased the pressor response to angiotensin II in C rats. In F rats (with or without insulin pretreatment), the pressor response to angiotensin II was higher than that in vehicle pre-treated C animals, but similar to that observed in C after insulin infusion. In C rats phospho-ERK 1/2 hypothalamic levels significantly increased after angiotensin II injection in insulin pretreated animals compared to vehicle pre-treated rats, suggesting that MAPK activation might be involved in insulin potentiation of blood pressure response to angiotensin II in the brain. Phospho-ERK 1/2 hypothalamic levels were significantly increased in vehicle treated F rats compared to C, suggesting that basal MAPK activation might play a role in the enhanced response to angiotensin II observed in these animals. Finally, in F rats, either after vehicle or insulin infusion, angiotensin II injection was associated with a similar increase in phospho-ERK 1/2 hypothalamic levels, comparable to that observed after angiotensin II injection in insulin pre-treated C animals. ERK 1/2 blockade significantly reduced MAP in F rats compared to C. Moreover, ERK 1/2 inhibition completely abolished the Ang II pressor response in F rats and in insulin pre-treated C animals. All these findings suggest that insulin–angiotensin II interaction at hypothalamic level might be involved in the increase in blood pressure observed in the insulin resistant state.
publishDate 2013
dc.date.none.fl_str_mv 2013-08
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/11336/17890
Mayer, Marcos Alejandro; Höcht, Christian; Giani, Jorge Fernando; Muñoz, Marina Cecilia; Carranza, A.; et al.; Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats; Elsevier Science; Regulatory Peptides; 185; 8-2013; 37-43
0167-0115
url http://hdl.handle.net/11336/17890
identifier_str_mv Mayer, Marcos Alejandro; Höcht, Christian; Giani, Jorge Fernando; Muñoz, Marina Cecilia; Carranza, A.; et al.; Central insulin–angiotensin II interaction in blood pressure regulation in fructose overloaded rats; Elsevier Science; Regulatory Peptides; 185; 8-2013; 37-43
0167-0115
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0167011513000876
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.regpep.2013.06.001
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
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dc.publisher.none.fl_str_mv Elsevier Science
publisher.none.fl_str_mv Elsevier Science
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
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