Contrasting effects of sleep fragmentation and angiotensin-II treatment upon pro-inflammatory responses of mice.

ABSTRACT: Disordered sleep promotes inflammation in brain and peripheral tissues, but the mechanisms that regulate these responses are poorly understood. One hypothesis is that activation of the sympathetic nervous system (SNS) from sleep loss elevates blood pressure to promote vascular sheer stress leading to inflammation. As catecholamines produced from SNS activation can directly regulate inflammation, we pharmacologically altered blood pressure using an alternative approach-manipulation of the renin-angiotensin system (RAS). Male C57BL6/J mice were treated with angiotensin or captopril to elevate and reduce blood pressure, respectively and then exposed to 24-h of sleep fragmentation (SF) or allowed to sleep (control). Pro- and anti-inflammatory cytokine gene expression and as endothelial adhesio

SUBMITTER: Ensminger DC 

PROVIDER: S-EPMC9427781 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature