Hypertension has been a major public health problem due to the high prevalence and disability and death rates of cardiovascular diseases that have been the focus of prevention and treatment at home and abroad and a common concern for the whole society. Sleep apnea syndrome, here mainly refers to obstructive sleep apnea (OSA), is a common sleep breathing disorder. It has been found that hypertension and sleep apnea have a high coexistence, with approximately 50% of OSA patients suffering from hypertension and nearly 30% of hypertensive patients also having OSA, and up to 83% of patients with intractable hypertension have OSA in combination, as early as 1976, when researchers observed an increase in nocturnal blood pressure in OSA patients and a persistent increase in daytime blood pressure in some patients. The association of OSA with hypertension was first considered in 1976. Since then, several clinical, epidemiological and basic studies have confirmed that OSA can cause and/or exacerbate hypertension and is associated with the development of hypertension. At least 30 million hypertensives in China are associated with obstructive sleep apnea OSA patients are a high prevalence of hypertension that cannot be ignored, and by extrapolating the prevalence of both, there are at least 30 million hypertensives in China that may be associated with OSA, and if the hypertension in this group of patients is relieved or even eradicated by treating OSA, this should become an important progress in the prevention and treatment of hypertension, potentially reduce the prevalence and complication rate of hypertension in general. The seventh report of the American Committee on Prevention, Treatment and Evaluation of Hypertension identified OSA as a major cause of hypertension, clearly stating that hypertension triggered by OSA is secondary to hypertension of clear etiology. Several studies with volunteers and different animal subjects have confirmed that intermittent hypoxia in the sleep apnea pattern can lead to sustained elevation of blood pressure through, among other mechanisms, impairment of vascular endothelial diastolic function by inflammation and oxidative stress, increased renin-angiotensin-aldosterone system activity, and enhanced sympathetic excitability. The Wisconsin Sleep Cohort Study confirmed a linear relationship between 24-hour blood pressure and sleep apnea hypoventilation index (AHI), and that this linear relationship was independent of confounding factors such as body mass index (BMI). In 2003, the Sleep Respiratory Diseases Group of the Chinese Medical Association’s Division of Respiratory Diseases investigated the prevalence of hypertension in OSA patients in 20 hospitals across China. The results showed that the prevalence of hypertension in the OSA population in China was nearly 50%, and there was a significant trend of increased blood pressure and non-ascending changes between morning and night. The study confirmed that the prevalence of hypertension and the degree of blood pressure elevation were clearly correlated with the severity of OSA. In addition, hypertension caused by OSA is not limited to adults; studies have shown that OSA has become an important cause of hypertension in children. Excision of tonsils and adenoids and continuous positive airway pressure ventilation (CPAP) treatment in children are more effective than in adult patients for hypertension. Studies have shown occult hypertension in up to 32% of patients with OSA. Another feature of hypertension in OSA patients is recalcitrant hypertension, and studies have confirmed that effective treatment of OSA is highly effective in controlling blood pressure in this group of hypertensive patients. Treatment of sleep apnea-associated hypertension High standards of thoroughness and efficacy of OSA treatment are emphasized Treatment of OSA and antihypertensive drug therapy are two aspects of treatment of sleep apnea-associated hypertension, and one cannot be separated from the other. Among them, OSA treatment includes treatments such as CPAP, surgery and oral appliances. Weight loss, postural therapy and some lifestyle interventions (e.g., smoking and alcohol cessation and bedtime sedation abstinence) are also effective, but only as treatment for patients with snoring, mild OSA and as adjunctive therapy for moderate to severe patients. Pharmacological treatment of hypertension has no clear efficacy on OSA itself. The reduction of blood pressure during the daytime in OSA patients by pharmacological treatment is certain, while the effect of lowering blood pressure at night is limited, and the treatment of OSA such as CPAP needs to be given at the same time. Cough and nasopharyngeal inflammation, which can be induced by some antihypertensive drugs, may aggravate OSA and increase the number of apneas in patients, which needs to be noted. The treatment of OSA in patients with sleep apnea-related hypertension emphasizes the thoroughness of OSA treatment and high standards of efficacy, i.e., the treatment must result in an AHI of less than 5 times/h and complete relief of sleep hypoxia, and only then can OSA treatment be evaluated for its role in lowering blood pressure. Currently, CPAP therapy is the first choice for OSA, especially for patients with OSA who also have hypertension. CPAP acts as a gas stent to open the upper airway that is obstructed during sleep for the purpose of treating OSA. The best current efficacy study confirmed that CPAP reduced daytime blood pressure by 10.3/11.2 mm Hg and nighttime blood pressure by 12.6/11.4 mm Hg. However, most studies have shown that CPAP is mildly effective in lowering daytime blood pressure and more effective in lowering nighttime hypertension. Patients with more severe OSA, difficult-to-control hypertension and better compliance with CPAP therapy had more blood pressure reduction after CPAP treatment. In patients with refractory hypertension, CPAP and oral appliances are effective in treating and reducing OSA and thus lowering blood pressure.