Obstructive sleep apnea (OSA) is considered a contributing factor to the development of hypertension and is especially associated with resistant hypertension and there is evidence that untreated OSA increases the risk of cardiovascular morbidity and mortality. Moreover, intermittent nocturnal hypoxia and hypoxemia, a pathognomic feature in OSA, might activate the renin-angiotensin system. There is also growing evidence to indicate that prolonged exposure to elevated aldosterone concentrations is associated with target organ damage in the heart, kidney, and arterial wall and with a high cardiovascular risk in patients with primary aldosteronism. It has been postulated that aldosterone worsens OSA by promoting the accumulation of fluid within then neck area, which then contributes to increased upper airway resistance. Therefore, it has been suggested that there might be a path of physiological link and overlap between PA and OSA.
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