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dc.contributor.author | González-Correa, Cristina | |
dc.contributor.author | Moleón, Javier | |
dc.contributor.author | Miñano, Sofía | |
dc.contributor.author | Robles-Vera, Iñaki | |
dc.contributor.author | Toral, Marta | |
dc.contributor.author | Martín-Morales, Natividad | |
dc.contributor.author | O'Valle, Francisco | |
dc.contributor.author | Sánchez, Manuel | |
dc.contributor.author | Gómez-Guzmán, Manuel | |
dc.contributor.author | Jiménez, Rosario | |
dc.contributor.author | Romero, Miguel | |
dc.contributor.author | Duarte, Juan | |
dc.date.accessioned | 2023-09-15T10:54:19Z | |
dc.date.available | 2023-09-15T10:54:19Z | |
dc.date.issued | 2023-02 | |
dc.identifier.citation | Biomed Pharmacother. 2023 Feb;158:114149. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/16469 | |
dc.description.abstract | Microbiota has a crucial role in the host blood pressure (BP) regulation. The present study analyzes whether the mineralocorticoid receptor antagonist spironolactone ameliorates the dysbiosic state in a genetic model of neurogenic hypertension. Twenty-week-old male Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were randomly allocated into three groups: untreated WKY, untreated SHR, and SHR treated with spironolactone for 5 weeks. Spironolactone restored the Firmicutes/Bacteroidetes proportion, and acetate-producing bacteria populations to WKY levels. Spironolactone reduced the percentage of intestinal aerobic bacteria. The amelioration of gut dysbiosis was linked to a reduction in the gut pathology, an enhanced colonic integrity, a reduced gut permeability and an attenuated sympathetic drive in the gut. Spironolactone was unable to reduce neuroinflammation and oxidative stress in the paraventricular nuclei in the hypothalamus. Spironolactone reduced the higher Th17 cells proportion in mesenteric lymph nodes and Th17 infiltration in aorta, improved aortic endothelial function and reduced systolic BP. This study demonstrates for the first time that spironolactone reduces gut dysbiosis in SHR. This effect could be related to its capability to improve gut integrity and pathology due to reduced sympathetic drive in the gut. | es_ES |
dc.description.sponsorship | This work was supported by Grants from Comision ´ Interministerial de Ciencia y Tecnología, Ministerio de Economía y competitividad (PID2020-116347RB-I00), and Junta de Andalucía (CTS 164, P20_00193, A-CTS-318-UGR20) with funds from the European Union, and by the Ministerio de Economia y Competitividad, Instituto de Salud Carlos III (CIBER-CV), Spain. M.T. and I.R.-V. are postdoctoral fellow of Instituto de Salud Carlos III (Juan de la Cierva Incorporacion ´ Program, and Juan de la Cierva Formacion ´ Program, respectively). J.M. is a predoctoral fellow of MINECO, and C.G.-C. and S.M. are predoctoral fellow of Junta de Andalucía. The cost of this publication was paid in part with funds from the European Union (Fondo Europeo de Desarrollo Regional, FEDER, “FEDER una manera de hacer Europa”). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject.mesh | Gastrointestinal Microbiome | es_ES |
dc.subject.mesh | Hypertension | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Male | es_ES |
dc.subject.mesh | Rats | es_ES |
dc.subject.mesh | Blood Pressure | es_ES |
dc.subject.mesh | Dysbiosis | es_ES |
dc.subject.mesh | Rats, Inbred SHR | es_ES |
dc.subject.mesh | Rats, Inbred WKY | es_ES |
dc.subject.mesh | Receptors, Mineralocorticoid | es_ES |
dc.subject.mesh | Spironolactone | es_ES |
dc.title | Mineralocorticoid receptor blockade improved gut microbiota dysbiosis by reducing gut sympathetic tone in spontaneously hypertensive rats. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 36566524 | es_ES |
dc.format.volume | 158 | es_ES |
dc.format.page | 114149 | es_ES |
dc.identifier.doi | 10.1016/j.biopha.2022.114149 | es_ES |
dc.contributor.funder | Ministerio de Economía y Competitividad (España) | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | Centro de Investigación Biomédica en Red - CIBERCV (Enfermedades Cardiovasculares) | es_ES |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1950-6007 | es_ES |
dc.relation.publisherversion | 10.1016/j.biopha.2022.114149 | es_ES |
dc.identifier.journal | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Inmunobiología | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Regulación Génica en Remodelado Vascular e Inflamación | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2020-116347RB-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/P20-00193 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/A-CTS-318-UGR20 | es_ES |