With the world-wide rise in obesity, the prevalence of obstructive sleep apnea has increased, which leads to disordered sleep patterns and consequently inflammation in brain and peripheral tissues. As hypertension is associated with obesity, it is unclear whether increased vascular sheer forces from elevated blood pressure promote inflammation during fragmented sleep. To test this possibility, we pharmacologically manipulated the renin-angiotensin system (RAS) of male C57BL6/j mice using angiotensin and captopril to elevate and reduce blood pressure, respectively. Mice were then exposed to 24 h of sleep fragmentation. Pro- and anti-inflammatory cytokine gene expression was measured in brain and peripheral tissues, as well as endothelial adhesion gene expression in heart and aorta, and serum glucocorticoids (corticosterone). RAS manipulation elevated cytokines and endothelial adhesion expression in heart and aorta while sleep fragmentation increased cytokine expression in brain and peripheral tissues. However, there were interactive effects of RAS manipulation and sleep fragmentation upon cytokine gene expression in hippocampus and hypothalamus, suggesting a potential role of blood pressure in altering neuroinflammation in response to sleep fragmentation. Sleep fragmentation, but not RAS manipulation, elevated serum corticosterone concentration. These findings highlight the contrasting effects of RAS manipulation and sleep fragmentation, implying that inflammation from sleep fragmentation is largely independent of RAS manipulation.

This data set is a combination of ELISA and real-time qPCR. As described in the methods section, the empirical data is from C57BL6/j mice that were pharmacologically manipulated with using angiotensin and captopril to elevate and reduce blood pressure, respectively, to assess the impact of  renin-angiotensin systems influence on the inflammatory response to sleep fragmentation.