Obstructive Sleep Apnea (OSA) and hypertension have a high rate of co-occurrence, with OSA being a causative factor for hypertension. Sympathetic activity due to intermittent hypoxia and/or fragmented sleep is the most important mechanisms triggering the elevation in blood pressure in OSA. OSA-related hypertension is characterized by resistant hypertension, nocturnal hypertension, abnormal blood pressure variability, and vascular remodeling. In particular, the prevalence of OSA is high in patients with resistant hypertension, and the mechanism proposed includes vascular remodeling due to the exacerbation of arterial stiffness by OSA. Continuous positive airway pressure therapy is effective at lowering blood pressure, however, the magnitude of the decrease in blood pressure is relatively modest, therefore, patients often need to also take antihypertensive medications to achieve optimal blood pressure control. Antihypertensive medications targeting sympathetic pathways or the renin-angiotensin-aldosterone system have theoretical potential in OSA-related hypertension, Therefore, beta-blockers and renin-angiotensin system inhibitors may be effective in the management of OSA-related hypertension, but current evidence is limited. The characteristics of OSA-related hypertension, such as nocturnal hypertension and obesity-related hypertension, suggests potential for angiotensin receptor-neprilysin inhibitor (ARNI), sodium-glucose cotransporter 2 inhibitors (SGLT2i) and glucose-dependent insulinotropic polypeptide receptor/ glucagon-like peptide-1 receptor agonist (GIP/GLP-1 RA). Recently, OSA has been considered to be caused not only by upper airway anatomy but also by several non-anatomic mechanisms, such as responsiveness of the upper airway response, ventilatory control instability, and reduced sleep arousal threshold. Elucidating the phenotypic mechanisms of OSA may potentially advance more personalized hypertension treatment strategies in the future.
