Under normal conditions, blood pressure is reduced after sleep, but in most patients with obstructive sleep apnea syndrome, blood pressure (including systolic and diastolic blood pressure) is significantly elevated after sleep, and after treatment of apnea syndrome, such as the application of continuous positive pressure ventilation treatment to achieve significant improvement, blood pressure is also significantly reduced, indicating that there is a causal relationship between the two. The mechanism is summarized as follows: sleep → apnea, respiratory dysfunction → hypoxia → decreased partial pressure of oxygen in blood → hypoxemia hypoxemia → stimulation of peripheral cardiovascular chemoreceptors → increased sympathetic excitability → increased secretion of catecholamines resulting in increased vasoconstriction, increased heart rate, increased cardiac contractility, increased cardiac output → increased blood pressure hypoxemia → activation of the renin-angiotensin system → increased production of angiotensin II → increased blood pressure. Increased production of angiotensin II → increased blood pressure. As seen above, the root cause of complications of hypertension is hypoxemia caused by apnea, and the longer the patient is in the hypoxic state, the more obvious the increase in blood pressure. In other words, the elevated nocturnal blood pressure in patients with obstructive sleep apnea syndrome is positively correlated with the hypoventilation index (AHI) of sleep apnea. Peripheral chemoreceptors are in the carotid sinus and have an important role in sympathetic nerve activity. It has been demonstrated that persistent hypertension can occur when animals are placed in a hypoxic environment, and that if the carotid sinus is preemptively removed from the animal before performing the experiment, no increase in blood pressure can be induced. Catecholamines are substances that cause strong constriction of fine arteries, which increases peripheral vascular resistance leading to increased blood pressure. It has also been observed that patients with obstructive sleep apnea syndrome not only have increased secretion of catecholamines during sleep, but also have higher than normal concentrations of catecholamines in the blood during the awakened state. In addition, other studies have reported that obstructive sleep apnea syndrome is not only complicated by hypertension, but is also a cause of primary hypertension.