| First Author | Caeiro X | Year | 2006 |
| Journal | Neuroscience | Volume | 142 |
| Issue | 2 | Pages | 557-65 |
| PubMed ID | 16887279 | Mgi Jnum | J:113139 |
| Mgi Id | MGI:3664667 | Doi | 10.1016/j.neuroscience.2006.06.024 |
| Citation | Caeiro X, et al. (2006) beta-Endorphin involvement in the regulatory response to body sodium overload. Neuroscience 142(2):557-65 |
| abstractText | 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 (betaend(-/-)), heterozygous (betaend(+/-)) and wild-type (betaend(+/+)) 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 betaend(-/-) mutant mice compared with betaend(+/+) mice kept in the same experimental conditions (P<0.01), but no statistical differences were observed between betaend(+/-) and betaend(+/+) 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, betaend(-/-) mice maintained on a HSD showed a significant increase in Fos-like immunoreactive neurons in the median preoptic nucleus (P<0.01) compared with betaend(+/-) and betaend(+/+) animals. Additionally, betaend(-/-) mice had higher levels of urinary epinephrine excretion (P<0.05) on a HSD in comparison to betaend(+/+) and betaend(+/-) 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. |
