The relationship between sleep apnea and blood pressure was examined in 7 patients with sleep apnea syndrome (SAS). In addition, whether or not SAS is a risk factor for cerebrovascular disease was assessed. Polysomnography, including measurements of arterial 02 saturation (Sa02), was performed in 7 patients during a 3-day hospitalization period; direct intra-arterial blood pressure was continuously recorded. The blood pressure data were analyzed at the beginning of apnea, the beginning of fall in Sa02, the end of apnea, the time of maximum blood pressure, and the time of Sa02 recovery. Analysis was also carried out for 30 s at 30-min intervals to assess nocturnal blood pressure variability.Two urine specimens, one accumulated from 9 a.m. to 9 p.m. and the other from 9 p.m. to 9 a.m., were collected. The pattern of blood pressure changes did not reveal the nocturnal decrease observed in normal subjects. A transient elevation of blood pressure was observed at the end of each apneic period; the mean increase in blood pressure was 28.0 mmHg in systole and 16.4 mmHg in diastole, and the maximum increase in systolic blood pressure was over 100 mmHg. There was no significant difference between diurnal and nocturnal concentrations of urinary catecholamines, suggesting that the sympathetic activity of patients with SAS is not decreased at night. Furthermore, the transient but considerable elevation of blood pressure observed at the end of each apneic period suggests that SAS may potentially trigger cerebrovascular disease. (Hypertens Res 1993;16: 209-213)