Zvartau N E, Conrady A O, Sviryaev Y V, Rotari O P, Merkulova N K, Kalinkin A L, Shlyakhto E V, Bagrov A Y
Almazov Research Institute of Cardiology, Saint-Petersburg, Russia.
Cell Mol Biol (Noisy-le-grand). 2006 Dec 30;52(8):24-7.
Although obstructive sleep apnea (OSA) is an independent risk factor for hypertension, the underlying mechanisms are not clearly understood. Apnea and hypopnea episodes during sleep lead to sympathoactivation, decrease plasma pH, and predispose to sodium and volume retention. We hypothesized that, the latter could stimulate digitalis-like natriuretic/vasopressor hormones, endogenous ouabain (EO) and marinobufagenin (MBG). Overnight polysomnography (Embletta) and 24 hrs blood pressure monitoring (SpaceLab 90207) was conducted in 52 consecutive patients with OSA (51 +/- 8 years; 40 males, 12 females) and in 48 age-matched hypertensive subjects without OSA. According to the polysomnography data, 17 patients had a mild degree of OSA (apnea/hypopnea index (AHI) 5-15), 17 patients-moderate (AHI 15-30) and 18 -severe OSA (AHI >30). Levels of MBG excretion co-varied with OSA severity (0.5 +/- 0.1, 0.9 +/- 0.04 and 1.2 +/- 0.06 nmoles per 24 hrs, respectively), while excretion of EO did not differ in patients with different degrees of OSA severity. Our observations suggest that MBG may be involved in the pathogenesis of hypertension in OSA, and may be a marker of OSA severity.
尽管阻塞性睡眠呼吸暂停(OSA)是高血压的一个独立危险因素,但其潜在机制尚不清楚。睡眠期间的呼吸暂停和呼吸浅慢发作会导致交感神经激活,降低血浆pH值,并易引发钠潴留和容量潴留。我们推测,后者可能会刺激洋地黄样利钠/血管加压激素、内源性哇巴因(EO)和海蟾蜍精(MBG)。对52例连续的OSA患者(51±8岁;40例男性,12例女性)和48例年龄匹配的无OSA的高血压患者进行了夜间多导睡眠图监测(Embletta)和24小时血压监测(SpaceLab 90207)。根据多导睡眠图数据,17例患者患有轻度OSA(呼吸暂停/呼吸浅慢指数(AHI)为5 - 15),17例患者为中度(AHI为15 - 30),18例患者为重度OSA(AHI>30)。MBG排泄水平与OSA严重程度呈共变关系(分别为每24小时0.5±0.1、0.9±0.04和1.2±0.06纳摩尔),而不同OSA严重程度患者的EO排泄无差异。我们的观察结果表明,MBG可能参与了OSA患者高血压的发病机制,并且可能是OSA严重程度的一个标志物。