β-Endorphin involvement in the regulatory response to body sodium overload

Abstract

The present study was performed to examine the role of the endogenous β-endorphinergic system on blood pressure regulation, sympathetic and brain activity during body sodium overload. β-Endorphin knockout (βend −/−), heterozygous (βend +/−) and wild-type (βend +/+) 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 βend −/− mutant mice compared with βend +/+ mice kept in the same experimental conditions ( P<0.01), but no statistical differences were observed between βend +/− and βend +/+ 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, βend −/− mice maintained on a HSD showed a significant increase in Fos-like immunoreactive neurons in the median preoptic nucleus ( P<0.01) compared with βend +/− and βend +/+ animals. Additionally, βend −/− mice had higher levels of urinary epinephrine excretion ( P<0.05) on a HSD in comparison to βend +/+ and βend +/− 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 β-endorphinergic system may play a part in the compensatory response to sodium overload, since the absence of β-endorphin causes an increase in systolic blood pressure, and increases median preoptic nucleus neural activity and urinary epinephrine excretion.