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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/22747
Ver los metadatos del registro completo
id |
CONICETDig_9f580b2539f783f7f66bc7ee8245f64b |
---|---|
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 |
_version_ |
1846782447024340992 |
score |
12.982451 |