“…The proposed mechanisms by which OSA leads to hypertension is believed to be apneas/hypopneas causing repetitive hypoxemia, nocturnal BP elevation and fluctuation and increased sympathetic activity, endothelial damage/dysfunction, oxidative stress, and hypertension target arterial damage; ie, increased arterial stiffness. 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 Recent studies have shown that nonmuscle myosin light chain kinase (nmMLCK) may be a key mechanism in intermittent hypoxia‐induced vascular oxidative stress and inflammation, both leading to functional and structural remodeling. 25 Furthermore, in hypertension, the presence of abdominal obesity or excessive fat deposition in the neck area, causes airway obstruction during sleep, and on molecular level leads to overproduction of adipokines, chronic low‐grade inflammation, and increased arterial stiffness.…”