In clinical work, obstructive sleep apnea hypoventilation syndrome is often combined with hypertension, and there is a correlation between the two. Studies have found that 45% to 48% of patients with obstructive sleep apnea hypoventilation syndrome also have hypertension, and more than 30% of patients with hypertension also have obstructive sleep apnea hypoventilation syndrome. Obstructive sleep apnea hypoventilation syndrome is considered to be an independent risk factor for the occurrence of cardiovascular and cerebrovascular diseases 1. It is often accompanied by snoring, sleep structure disorder, hypoxemia, daytime drowsiness, inattention and other phenomena, and can lead to cardiac, cerebral and pulmonary vascular comorbidities. 2. Characteristics of hypertension combined with obstructive sleep apnea hypoventilation syndrome Some studies have shown that the blood pressure level of hypertensive patients with obstructive sleep apnea hypoventilation syndrome is increased in the early morning and at night, and the circadian rhythm of blood pressure deteriorates to non-arytenoidal or even anti-arytenoidal. The circadian blood pressure rhythm change is an independent predictor of cardiovascular events. 3, the relationship between obstructive sleep apnea hypoventilation syndrome combined with refractory hypertension obstructive sleep apnea hypoventilation syndrome combined with hypertension is often refractory hypertension, the incidence of refractory hypertension reached 43% to 47%, most of the diastolic blood pressure is mainly elevated. Obstructive sleep apnea hypoventilation syndrome is an independent risk factor for refractory hypertension, and the presence of obstructive sleep apnea hypoventilation syndrome aggravates the difficulty of treatment of refractory hypertension. 4, obstructive sleep apnea hypoventilation syndrome combined with the mechanism leading to hypertension Mechanism: ① intermittent hypoxemia and hypercapnia cause increased sympathetic nerve activity, activation of the renin-angiotensin II-aldosterone system in vivo, increased plasma catecholamine levels, and increased peripheral vascular resistance leading to hypertension. (ii) Increased apnea hypoventilation index and decreased oxygen saturation in patients with obstructive sleep apnea hypoventilation syndrome accelerate the apoptosis of vascular endothelial cells, which in turn impairs the function of endothelium-dependent vasodilatory substances and disrupts the balance between vasodilatory and vasoconstrictive substances, causing an increase in blood pressure. ③Repeated hypoxia stimulates the release of inflammatory substances and the enhancement of oxidative stress, which increases vascular endothelial destruction. ④Chronic intermittent hypoxemia causes increased blood glucose and insulin resistance through excitation of sympathetic nerves and stimulation of secretion of various hormones, which weakens the diastolic function of insulin-regulated vascular endothelium. ⑤ In addition, there are many factors such as mechanical effects caused by increased negative pressure in the thoracic cavity, genetics, and age. 5.Treatment Device therapy: In addition to general anti-hypertensive drugs, continuous positive airway pressure ventilation (CPAP) is an effective treatment for anatomical factors as the first-line treatment option for obstructive sleep apnea hypoventilation syndrome. Drug therapy: acetazolamide is a carbonic anhydrase inhibitor that improves breathing disorders and sleep quality by stimulating ventilation. The sulfonyl group in the antiepileptic drug zonisamide also has a carbonic anhydrase inhibitory effect. Carbonic anhydrase inhibitors can relieve sleep apnea symptoms in patients with obstructive sleep apnea hypoventilation syndrome, and also control weight in obese patients. Interventional therapy: Renal denervation with catheters may lower blood pressure and improve the severity of obstructive sleep apnea hypoventilation syndrome in patients with intractable hypertension.