Previous human, animal, and in vitro studies show that chronic intermittent hypoxia, a pathophysiological manifestation in OSA, induces sympathetic outflow to the kidney, stimulates renin release, and leads to elevated circulating levels of angiotensin II (Ang II) (41, 42), both of which are important regulators for aldosterone secretion from the adrenal gland. This evidence concerns the gene REN and obstructive sleep apnea syndrome.