Obstructive sleep apnea (OSA) is characterized by recurrent complete (apneas) and partial (hypopneas) upper airway obstructive events, resulting in intermittent hypoxemia, autonomic fluctuation, and sleep fragmentation. OSA has been associated with a number of cardiovascular complications, including hypertension, AF and other arrhythmias, HF, coronary artery disease, stroke, PH, metabolic syndrome, diabetes, and cardiovascular mortality. Notably, OSA is a condition with potential for negative feedback in which it worsens conditions that may in turn worsen the OSA (e.g., OSA → hypertension → worsened OSA). OSA is highly prevalent in hypertensive patients, of whom 30% to 50% will have comorbid OSA. This is especially true in patients with resistant hypertension, among whom up to 80% may have OSA. Although OSA has been implicated as an independent risk factor for hypertension and resistant hypertension, effects of continuous positive airway pressure (CPAP) therapy on blood pressure (BP) lowering in hypertensive patients with OSA have been disappointing and inconsistent, with a meta-analysis showing reductions of BP of between 2- and 3-mm Hg. CPAP adherence is associated with greater reductions in nocturnal BP. Even in patients with OSA with resistant hypertension, a 3-month treatment with CPAP (versus no CPAP) reduced 24 hour systolic, mean, and diastolic BPs by ≈3 mm Hg, with a significant correlation between hours of CPAP use and BP reduction. BP normally decreases during sleep. Although the degree of nighttime BP dipping has a normal distribution in a population setting, an arbitrary cut-off has been proposed to define patients as ‘dippers’ if their nocturnal BP falls by >10% of the daytime average BP value; however, the ‘dipping’ status is often highly variable from day to day and thus is poorly reproducible.