[Role of sympathetic nerve activity and arterial endothelial function in pathogenesis of hypertension in patients with obstructive sleep apnea-hypopnea syndrome].

Objective: To explore the role of sympathetic nerve activity and vessel endothelial function in the pathogenesis of hypertension in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS).

Methods: Based on polysomnography (PSG), blood pressure (BP) and disease history, 93 subjects were divided into four groups: OSAHS with hypertension (OH), OSAHS without hypertension (O), hypertension without OSAHS (H), normal control (N). In addition to the blood pressure measurement, blood samples were collected before and after sleep during the PSG testing night to measure norepinephrine, endothelin, and NO levels. Urine samples were also collected during this time to test the level of vanillyl mandalic acid (VMA).

Results: Patients in OH group and O group had significantly increased plasma NE value (P < 0.05) in the next morning compared with those before sleep and the change was more significant in OH group compared to O group (P < 0.01). Pre-and after-sleep urine VMA levels in all groups showed no significant differences. Plasma NE and ET levels in OSAHS with and without hypertension after sleep were positively correlated with mean arterial pressure (MAP), apnea-hypopnea index (AHI), number of oxygen desaturation >or= 4% per hour (ODI(4)), percentage of time of oxygen saturation lower than 90% (T90) and correlated negatively with minimum arterial oxygen saturation (minSaO(2)) and mean arterial oxygen saturation (MSaO(2)). Moreover, plasma ET also correlated positively with MAP, AHI, maximum apnea time, total apnea time. Compared with other groups plasma ET value increased significantly and serum NO value decreased in the next morning in both O and OH group. Serum NO value after one night sleep in both hypertensive and norhypertensive OSAHS patients was negatively correlated with MAP, AHI, maximum apnea time, total apnea time, ODI(4), T90, and positively with minSaO(2) and MSaO(2).

Conclusions: Sympathetic nerve activation and endothelial dysfuntion characterized by an imbalance of endothelium-derived systolic and diastolic factors may play an important role in the development of transient and sustained increase of blood pressure in patients with OSAHS.