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dc.contributor.author
Caeiro, Ximena Elizabeth  
dc.contributor.author
Hansen, C.  
dc.contributor.author
García, N.  
dc.contributor.author
Vivas, Laura Marta  
dc.date.available
2024-08-07T12:01:13Z  
dc.date.issued
2006-10  
dc.identifier.citation
Caeiro, Ximena Elizabeth; Hansen, C.; García, N.; Vivas, Laura Marta; β-Endorphin involvement in the regulatory response to body sodium overload; Pergamon-Elsevier Science Ltd; Neuroscience; 142; 2; 10-2006; 557-565  
dc.identifier.issn
0306-4522  
dc.identifier.uri
http://hdl.handle.net/11336/241979  
dc.description.abstract
The present study was performed to examine the role of the endogenous beta-endorphinergic system on blood pressure regulation, sympathetic and brain activity during body sodium overload. Beta-endorphin knockout (beta end-/-), heterozygous (beta end+/-) and wild-type (beta end+/+) mice were submitted for two weeks to either a normal- or a high-sodium diet (NSD and HSD, respectively), and systolic blood pressure (SBP), urinary catecholamines (as an index of sympathetic nervous system activity), and the brain pattern of Fos-like immunoreactivity (as a marker of neuronal activation) were evaluated in each group. HSD caused a significant increase in SBP in beta end-/- mutant mice compared with beta end+/+ mice kept in the same experimental conditions (P < 0.01), but no statistical differences were observed between beta end+/- and beta end+/+ on a HSD. Moreover, when animals from the three genetic lines were fed with a NSD no changes in SBP were evidenced. With regard to brain activity, beta end-/- mice maintained on a HSD showed a significant increase in Fos-like immunoreactive neurons in the median preoptic nucleus (P < 0.01) compared with beta end+/- and beta end+/+ animals. Additionally, beta end-/- mice had higher levels of urinary epinephrine excretion (P < 0.05) on a HSD in comparison to beta end+/+ and beta end+/- animals in the same experimental conditions. No differences, however, were registered in norepinephrine and dopamine urinary excretion in animals from the three genetic lines after two weeks on either a HSD or a NSD. In summary, our results indicate that the beta-endorphinergic system may play a part in the compensatory response to sodium overload, since the absence of beta-endorphin causes an increase in systolic blood pressure, and increases median preoptic nucleus neural activity and urinary epinephrine excretion.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Pergamon-Elsevier Science Ltd  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Blood Pressure  
dc.subject
High Sodium Diet  
dc.subject.classification
Fisiología  
dc.subject.classification
Medicina Básica  
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
β-Endorphin involvement in the regulatory response to body sodium overload  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2024-08-05T14:02:46Z  
dc.journal.volume
142  
dc.journal.number
2  
dc.journal.pagination
557-565  
dc.journal.pais
Estados Unidos  
dc.description.fil
Fil: Caeiro, Ximena Elizabeth. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina  
dc.description.fil
Fil: Hansen, C.. No especifíca;  
dc.description.fil
Fil: García, N.. No especifíca;  
dc.description.fil
Fil: Vivas, Laura Marta. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; Argentina  
dc.journal.title
Neuroscience  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0306452206008530  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.neuroscience.2006.06.024