The underlying mechanism centers on dysregulated secretion of atrial natriuretic peptide (ANP).[26] ANP, synthesized and released by atrial myocytes, antagonizes the renin–angiotensin–aldosterone axis and sympathetic outflow while promoting renal sodium and water excretion.[27] In OSAHS, nocturnal increases in intrathoracic negative pressure, intermittent hypoxia, hypercapnia, and sleep fragmentation evoke surges in sympathetic activity and systemic/pulmonary vasoconstriction, thereby augmenting cardiac preload. The gene discussed is REN; the disease is obstructive sleep apnea syndrome.