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Cardiac adverse effects of naloxone-precipitated morphine withdrawal on right ventricle: Role of corticotropin-releasing factor (CRF) 1 receptor

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dc.contributor.authorNavarro Zaragoza, Javier
dc.contributor.authorMartínez Laorden, Elena
dc.contributor.authorMora, L.
dc.contributor.authorHidalgo, J.
dc.contributor.authorLaorden Carrasco, María Luisa
dc.contributor.authorMilanés Maquilón, María Victoria
dc.contributor.departmentFarmacología
dc.date.accessioned2026-01-23T16:49:47Z
dc.date.available2026-01-23T16:49:47Z
dc.date.copyright© 2014, Elsevier Inc. All rights reserved
dc.date.issued2014-01-05
dc.description.abstractOpioid addiction is associated with cardiovascular disease. However, mechanisms linking opioid addiction and cardiovascular disease remain unclear. This study investigated the role of corticotropin-releasing factor (CRF) 1 receptor in mediating somatic signs and the behavioural states produced during withdrawal from morphine dependence. Furthermore, it studied the efficacy of CRF1 receptor antagonist, CP-154,526 to prevent the cardiac sympathetic activity induced by morphine withdrawal. In addition, tyrosine hydroxylase (TH) phosphorylation pathways were evaluated. Like stress, morphine withdrawal induced an increase in the hypothalamic–pituitary–adrenal (HPA) axis activity and an enhancement of noradrenaline (NA) turnover. Pre-treatment with CRF1 receptor antagonist significantly reduced morphine withdrawal-induced increases in plasma adrenocorticotropic hormone (ACTH) levels, NA turnover and TH phosphorylation at Ser31 in the right ventricle. In addition, CP-154,526 reduced the phosphorylation of extracellular signal-regulated kinase (ERK) after naloxone-precipitated morphine withdrawal. In addition, CP-154,526 attenuated the increases in body weight loss during morphine treatment and suppressed some of morphine withdrawal signs. Altogether, these results support the idea that cardiac sympathetic pathways are activated in response to naloxone-precipitated morphine withdrawal suggesting that treatment with a CRF1 receptor antagonist before morphine withdrawal would prevent the development of stress-induced behavioural and autonomic dysfunction in opioid addicts.
dc.formatapplication/pdf
dc.format.extent8
dc.identifier.citationToxicology and Applied Pharmacology 275 (2014) 28–35
dc.identifier.doihttps://doi.org/10.1016/j.taap.2013.12.021
dc.identifier.issn0041-008X
dc.identifier.urihttp://hdl.handle.net/10201/192450
dc.languageeng
dc.publisherElsevier
dc.relationThis research was supported by grants from the Ministerio de Ciencia e Innovación (Grant SAF/FEDER 2010-17907), and Red de Trastornos Adicitivos (RETICS RD12/0028//0003).
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0041008X13005747?via%3Dihub
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectMorphine withdrawal
dc.subjectHypothalamus–pituitary–adrenocortical axis
dc.subjectNoradrenaline turnover
dc.subjectExtracellular signal-regulated kinase
dc.subjectRight ventricle
dc.subjectTyrosine hydroxylase
dc.subject.odsObjetivo 3: Salud
dc.titleCardiac adverse effects of naloxone-precipitated morphine withdrawal on right ventricle: Role of corticotropin-releasing factor (CRF) 1 receptor
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublicationes
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relation.isAuthorOfPublication.latestForDiscovery91a9c0cf-0115-4c34-9b53-72a417c2d883
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