Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors

Autores
Silva, Guillermo Benjamin; Atchison, Douglas K.; Juncos, Luis Isaias; Garcia, Nestor Horacio
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The energy required for active Na chloride reabsorption in the thick ascending limb (TAL) depends on oxygen consumption and oxidative phosphorylation (OXP). In other cells, Na transport is inhibited by the endogenous cannabinoid anandamide through the activation of the cannabinoid receptors (CB) type 1 and 2. However, it is unclear whether anandamide alters TAL transport and the mechanisms that could be involved. We hypothesized that anandamide inhibits TAL transport via activation of CB1 receptors and NO. For this, we measured oxygen consumption (QO2) in TAL suspensions to monitor the anandamide effects on transport and OXP. Anandamide reduced QO2 in a concentration-dependent manner. During Na-K-2Cl cotransport and Na/H exchange inhibition, anandamide did not inhibit TAL QO2. To test the role of the cannabinoid receptors, we used specific agonists and antagonists of CB1 and CB2 receptors. The CB1-selective agonist WIN55212–2 reduced QO2 in a concentration-dependent manner. Also, the CB1 receptor antagonist rimonabant blocked the effect of anandamide on QO2. In contrast, the CB2-selective agonist JHW-133 had no effect on QO2, while the CB2 receptor antagonist AM-630 failed to block the anandamide effects on QO2. To confirm these results, we measured CB1 and CB2 receptor expression and only CB1 expression was detected. Because CB1 receptors are strong nitric oxide synthase (NOS) stimulators and NO inhibits transport in TALs, we evaluated the role of NO. Anandamide stimulated NO production and the NOS inhibitor NG-nitro-l-arginine methyl ester blocked the anandamide effects on QO2. We conclude that anandamide inhibits TAL Na transport-related QO2 via activation of CB1 receptor and NOS.
Fil: Silva, Guillermo Benjamin. Universidad Católica de Córdoba; Argentina. Fundación Robert Cade; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Atchison, Douglas K.. Wayne State University; Estados Unidos. Henry Ford Hospital; Estados Unidos
Fil: Juncos, Luis Isaias. Fundación Robert Cade; Argentina
Fil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Materia
Nkcc2
Diuretics
Tubular Transport
Molecular Phisiology
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:11336/22747

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oai_identifier_str oai:ri.conicet.gov.ar:11336/22747
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptorsSilva, Guillermo BenjaminAtchison, Douglas K.Juncos, Luis IsaiasGarcia, Nestor HoracioNkcc2DiureticsTubular TransportMolecular Phisiologyhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The energy required for active Na chloride reabsorption in the thick ascending limb (TAL) depends on oxygen consumption and oxidative phosphorylation (OXP). In other cells, Na transport is inhibited by the endogenous cannabinoid anandamide through the activation of the cannabinoid receptors (CB) type 1 and 2. However, it is unclear whether anandamide alters TAL transport and the mechanisms that could be involved. We hypothesized that anandamide inhibits TAL transport via activation of CB1 receptors and NO. For this, we measured oxygen consumption (QO2) in TAL suspensions to monitor the anandamide effects on transport and OXP. Anandamide reduced QO2 in a concentration-dependent manner. During Na-K-2Cl cotransport and Na/H exchange inhibition, anandamide did not inhibit TAL QO2. To test the role of the cannabinoid receptors, we used specific agonists and antagonists of CB1 and CB2 receptors. The CB1-selective agonist WIN55212–2 reduced QO2 in a concentration-dependent manner. Also, the CB1 receptor antagonist rimonabant blocked the effect of anandamide on QO2. In contrast, the CB2-selective agonist JHW-133 had no effect on QO2, while the CB2 receptor antagonist AM-630 failed to block the anandamide effects on QO2. To confirm these results, we measured CB1 and CB2 receptor expression and only CB1 expression was detected. Because CB1 receptors are strong nitric oxide synthase (NOS) stimulators and NO inhibits transport in TALs, we evaluated the role of NO. Anandamide stimulated NO production and the NOS inhibitor NG-nitro-l-arginine methyl ester blocked the anandamide effects on QO2. We conclude that anandamide inhibits TAL Na transport-related QO2 via activation of CB1 receptor and NOS.Fil: Silva, Guillermo Benjamin. Universidad Católica de Córdoba; Argentina. Fundación Robert Cade; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Atchison, Douglas K.. Wayne State University; Estados Unidos. Henry Ford Hospital; Estados UnidosFil: Juncos, Luis Isaias. Fundación Robert Cade; ArgentinaFil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaAmerican Physiological Society2013-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/22747Silva, Guillermo Benjamin; Atchison, Douglas K.; Juncos, Luis Isaias; Garcia, Nestor Horacio; Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors; American Physiological Society; American Journal Of Physiology-renal Physiology; 304; 4; 2-2013; 376-3811931-857X1522-1466CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1152/ajprenal.00239.2012info:eu-repo/semantics/altIdentifier/url/http://ajprenal.physiology.org/content/304/4/F376info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:07:56Zoai:ri.conicet.gov.ar:11336/22747instacron: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:34982025-10-22 12:07:56.95CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
title Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
spellingShingle Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
Silva, Guillermo Benjamin
Nkcc2
Diuretics
Tubular Transport
Molecular Phisiology
title_short Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
title_full Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
title_fullStr Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
title_full_unstemmed Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
title_sort Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors
dc.creator.none.fl_str_mv Silva, Guillermo Benjamin
Atchison, Douglas K.
Juncos, Luis Isaias
Garcia, Nestor Horacio
author Silva, Guillermo Benjamin
author_facet Silva, Guillermo Benjamin
Atchison, Douglas K.
Juncos, Luis Isaias
Garcia, Nestor Horacio
author_role author
author2 Atchison, Douglas K.
Juncos, Luis Isaias
Garcia, Nestor Horacio
author2_role author
author
author
dc.subject.none.fl_str_mv Nkcc2
Diuretics
Tubular Transport
Molecular Phisiology
topic Nkcc2
Diuretics
Tubular Transport
Molecular Phisiology
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The energy required for active Na chloride reabsorption in the thick ascending limb (TAL) depends on oxygen consumption and oxidative phosphorylation (OXP). In other cells, Na transport is inhibited by the endogenous cannabinoid anandamide through the activation of the cannabinoid receptors (CB) type 1 and 2. However, it is unclear whether anandamide alters TAL transport and the mechanisms that could be involved. We hypothesized that anandamide inhibits TAL transport via activation of CB1 receptors and NO. For this, we measured oxygen consumption (QO2) in TAL suspensions to monitor the anandamide effects on transport and OXP. Anandamide reduced QO2 in a concentration-dependent manner. During Na-K-2Cl cotransport and Na/H exchange inhibition, anandamide did not inhibit TAL QO2. To test the role of the cannabinoid receptors, we used specific agonists and antagonists of CB1 and CB2 receptors. The CB1-selective agonist WIN55212–2 reduced QO2 in a concentration-dependent manner. Also, the CB1 receptor antagonist rimonabant blocked the effect of anandamide on QO2. In contrast, the CB2-selective agonist JHW-133 had no effect on QO2, while the CB2 receptor antagonist AM-630 failed to block the anandamide effects on QO2. To confirm these results, we measured CB1 and CB2 receptor expression and only CB1 expression was detected. Because CB1 receptors are strong nitric oxide synthase (NOS) stimulators and NO inhibits transport in TALs, we evaluated the role of NO. Anandamide stimulated NO production and the NOS inhibitor NG-nitro-l-arginine methyl ester blocked the anandamide effects on QO2. We conclude that anandamide inhibits TAL Na transport-related QO2 via activation of CB1 receptor and NOS.
Fil: Silva, Guillermo Benjamin. Universidad Católica de Córdoba; Argentina. Fundación Robert Cade; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Atchison, Douglas K.. Wayne State University; Estados Unidos. Henry Ford Hospital; Estados Unidos
Fil: Juncos, Luis Isaias. Fundación Robert Cade; Argentina
Fil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
description The energy required for active Na chloride reabsorption in the thick ascending limb (TAL) depends on oxygen consumption and oxidative phosphorylation (OXP). In other cells, Na transport is inhibited by the endogenous cannabinoid anandamide through the activation of the cannabinoid receptors (CB) type 1 and 2. However, it is unclear whether anandamide alters TAL transport and the mechanisms that could be involved. We hypothesized that anandamide inhibits TAL transport via activation of CB1 receptors and NO. For this, we measured oxygen consumption (QO2) in TAL suspensions to monitor the anandamide effects on transport and OXP. Anandamide reduced QO2 in a concentration-dependent manner. During Na-K-2Cl cotransport and Na/H exchange inhibition, anandamide did not inhibit TAL QO2. To test the role of the cannabinoid receptors, we used specific agonists and antagonists of CB1 and CB2 receptors. The CB1-selective agonist WIN55212–2 reduced QO2 in a concentration-dependent manner. Also, the CB1 receptor antagonist rimonabant blocked the effect of anandamide on QO2. In contrast, the CB2-selective agonist JHW-133 had no effect on QO2, while the CB2 receptor antagonist AM-630 failed to block the anandamide effects on QO2. To confirm these results, we measured CB1 and CB2 receptor expression and only CB1 expression was detected. Because CB1 receptors are strong nitric oxide synthase (NOS) stimulators and NO inhibits transport in TALs, we evaluated the role of NO. Anandamide stimulated NO production and the NOS inhibitor NG-nitro-l-arginine methyl ester blocked the anandamide effects on QO2. We conclude that anandamide inhibits TAL Na transport-related QO2 via activation of CB1 receptor and NOS.
publishDate 2013
dc.date.none.fl_str_mv 2013-02
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/11336/22747
Silva, Guillermo Benjamin; Atchison, Douglas K.; Juncos, Luis Isaias; Garcia, Nestor Horacio; Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors; American Physiological Society; American Journal Of Physiology-renal Physiology; 304; 4; 2-2013; 376-381
1931-857X
1522-1466
CONICET Digital
CONICET
url http://hdl.handle.net/11336/22747
identifier_str_mv Silva, Guillermo Benjamin; Atchison, Douglas K.; Juncos, Luis Isaias; Garcia, Nestor Horacio; Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors; American Physiological Society; American Journal Of Physiology-renal Physiology; 304; 4; 2-2013; 376-381
1931-857X
1522-1466
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1152/ajprenal.00239.2012
info:eu-repo/semantics/altIdentifier/url/http://ajprenal.physiology.org/content/304/4/F376
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
application/pdf
dc.publisher.none.fl_str_mv American Physiological Society
publisher.none.fl_str_mv American Physiological Society
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
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