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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.
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January 1998,
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Journal of clinical hypertension (Greenwich, Conn.),
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Internal and emergency medicine,
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Zhonghua xin xue guan bing za zhi,
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