Obstructive Sleep Apnea and Hypertension: Is Aldosterone Blockade the Optimal Approach to Control Blood Pressure and Improve Oxygenation?

purpose of reviewObstructive sleep apnea (OSA) is common and strongly linked with systemic hypertension, including resistant and nocturnal forms. Traditional OSA therapies lead to modest blood pressure (BP) reductions, but optimal antihypertensive strategies in this population remain unclear. This review examines OSA driven hypertension mechanisms, differential responses to standard OSA therapies, and evaluates evidence for mineralocorticoid-targeted treatment - including blockade of aldosterone - as a tailored BP lowering and airway improving strategy. RECENT

findingsOSA promotes hypertension via intermittent hypoxia, sympathetic overactivity, sleep fragmentation, renin-angiotensin-aldosterone system (RAAS)-mediated fluid retention, and nocturnal fluid shifts that increase airway collapsibility. While continuous positive airway pressure (CPAP), oral appliances, weight loss, and other standard OSA therapies consistently yield modest BP reductions (typically 2-5 mmHg), patients with resistant hypertension, obesity, or high CPAP adherence derive greater benefit. Recent clinical studies demonstrate that mineralocorticoid receptor antagonists (MRAs) such as spironolactone or eplerenone reduce both apnea-hypopnea index (AHI) and BP in OSA patients with resistant hypertension. Emerging data from trials of selective aldosterone synthase inhibitors (ASIs) support meaningful BP reduction in obese hypertensive individuals with data on OSA specific outcomes remain forthcoming.