title: Beta-endorphin involvement in the regulatory response to body sodium overload.
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.
authors.affiliation: Instituto de Investigación Médica Mercedes y Martín Ferreyra, Casilla de correo 389, 5000 Córdoba, Argentina.
authors.forename: X
authors.initials: X
authors.lastname: Caeiro
authors.forename: C
authors.initials: C
authors.lastname: Hansen
authors.forename: N
authors.initials: N
authors.lastname: García
authors.forename: L
authors.initials: L
authors.lastname: Vivas
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal; D001794:Blood Pressure / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D001835:Body Weight / Q000187:drug effects / Q000235:genetics; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002395:Catecholamines / Q000652:urine; D003404:Creatinine / Q000652:urine; D004326:Drinking / Q000187:drug effects / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D007150:Immunohistochemistry / Q000379:methods; D051379:Mice; D018345:Mice, Knockout; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D012982:Sodium, Dietary / Q000378:metabolism* / Q000494:pharmacology; D001615:beta-Endorphin / Q000172:deficiency / Q000502:physiology*
chemical_list: D002395:Catecholamines; D016760:Proto-Oncogene Proteins c-fos; D012982:Sodium, Dietary; D001615:beta-Endorphin; D003404:Creatinine