Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for hypertension and cardiovascular disease. OSAS is the frequent underlying disease of secondary hypertension and resistant hypertension. OSAS increases both daytime and night-time ambulatory blood pressures through the activation of various neurohumoral factors including the sympathetic nervous system and the renin-angiotensin-aldosterone system. In particular, OSAS predominantly increases ambulatory BP during sleep compared with the awake period, with the result that OSAS is likely to be associated with the non-dipping pattern (diminished nocturnal BP fall) or riser pattern (higher sleep BP than awake BP) of nocturnal BP. An additional characteristic of ABP in OSAS is increased BP variability. The newly developed non-invasive hypoxia-trigger BP-monitoring system detected marked midnight BP surges (ranging from around 10 to 100 mm Hg) during sleep in OSAS patients. The exaggerated BP surge may trigger OSAS-related cardiovascular events occurring during sleep. Clinically, as nocturnal hypoxia is the determinant of morning minus evening BP difference (ME difference), OSAS should be strongly suspected when morning BP cannot be controlled <135/85 mm Hg with increased ME difference even by the specific antihypertensive medications targeting morning hypertension such as bedtime dosing of antihypertensive drugs. Understanding the characteristics of OSAS-related hypertension is essentially important to achieve perfect BP control over a 24-h period, including the sleep period, for more effective prevention of cardiovascular disease.