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Emerging evidence has supported a role of inflammation and immunity in the genesis of hypertension. In humans and experimental models of hypertension, cells of the innate and adaptive immune system enter target tissues, including vessels and the kidney, and release powerful mediators including cytokines, matrix metalloproteinases and reactive oxygen species that cause tissue damage, fibrosis and dysfunction. These events augment the blood pressure elevations in hypertension and promote end-organ damage. Factors that activate immune cells include sympathetic outflow, increased sodium within microenvironments where these cells reside, and signals received from the vasculature. In particular, the activated endothelium releases reactive oxygen species and interleukin (IL)-6 which in turn stimulate transformation of monocytes to become antigen presenting cells and produce cytokines like IL-1β and IL-23, which further affect T cell function to produce IL-17A. Genetic deletion or neutralization of these cytokines ameliorates hypertension and end-organ damage. In this review, we will consider in depth features of the hypertensive milieu that lead to these events and consider new treatment approaches to limit the untoward effects of inflammation in hypertension., (© 2021. The Author(s), under exclusive licence to Springer Nature Limited.)

Obstructive Sleep Apnea (OSA) is a common condition characterized by intermittent collapse of the upper airway during sleep, resulting in partial (hypopnoeas) and total obstructions (apneas). These respiratory events observed in OSA may trigger multiple pathways involved in the blood pressure (BP) instability during the night and potentially influencing daytime BP as well (carry-over effects). This review provides an update about the impact of OSA and its treatments on 24-h BP control. Overall, there is growing evidence suggest that OSA is associated with higher frequency of nondipping BP pattern and nocturnal hypertension in a dose-dependent manner. The presence of nondiping BP (especially the reverse pattern) is independently associated with OSA regardless of sleep-related symptoms suggesting a potential tool for screening OSA in patients with clinical indication for performing ABPM. Beyond dipping BP, preliminary evidence associated OSA with white-coat effect and higher frequency of masked hypertension and BP variability than the control group (no OSA). Unfortunately, most of the evidence on the evidence addressing the impact of OSA treatment on BP was limited to office measurements. In the last years, data from observational and randomized studies pointed that CPAP is able to promote 24-h BP decrease especially in patients with resistant and refractory hypertension. A randomized trial suggests that CPAP is able to decrease the rate of masked hypertension as compared to no treatment in patients with severe OSA. Interestingly, nondipping BP is a good predictor of BP response to CPAP making ABPM an interesting tool for better OSA management.