Calhoun David A, Nishizaka Mari K, Zaman Mohammad A, Harding Susan M
Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA.
Chest. 2004 Jan;125(1):112-7. doi: 10.1378/chest.125.1.112.
The severity of obstructive sleep apnea (OSA) correlates with the difficulty of controlling BP. The mechanism, however, by which sleep apnea contributes to the development of resistant hypertension remains obscure. Having observed a high prevalence of OSA among hypertensive subjects with primary hyperaldosteronism, we hypothesized a possible association between sleep apnea and aldosterone excretion.
In consecutive subjects referred to a university clinic for resistant hypertension, we prospectively determined plasma renin activity (PRA), plasma aldosterone concentration (PAC), and 24-h urinary aldosterone excretion during high dietary salt ingestion. In addition, all subjects completed the Berlin Questionnaire, a survey designed to identify subjects at risk of having sleep apnea. Primary hyperaldosteronism (PA) was defined as a PRA < 1.0 ng/mL/h and 24-h urinary aldosterone excretion > 12 micro g during high urinary sodium excretion (> 200 mEq/24 h).
Of the 114 subjects evaluated, 72 subjects had a high probability and 42 subjects had a low probability of having sleep apnea based on their responses to the Berlin Questionnaire. Subjects at high risk for sleep apnea were almost two times more likely to have PA diagnosed (36 vs 19%, p < 0.05), tended to have lower PRA (1.2 +/- 1.8 ng/mL/h vs 1.9 +/- 4.1 ng/mL/h), and had significantly greater 24-h urinary aldosterone excretion (13.6 +/- 9.6 micro g vs 9.8 +/- 7.6 micro g, p < 0.05) compared to subjects at low risk of sleep apnea.
These data provide evidence of increased aldosterone excretion in subjects with resistant hypertension and symptoms of sleep apnea. While the causality of this association is unknown, it is hypothesized that sleep apnea contributes to the development of resistant hypertension by stimulating aldosterone excretion.
阻塞性睡眠呼吸暂停（OSA）的严重程度与血压控制难度相关。然而，睡眠呼吸暂停导致顽固性高血压发生的机制仍不清楚。在患有原发性醛固酮增多症的高血压患者中观察到OSA的高患病率后，我们推测睡眠呼吸暂停与醛固酮排泄之间可能存在关联。
在连续转诊至大学诊所治疗顽固性高血压的患者中，我们前瞻性地测定了高盐饮食期间的血浆肾素活性（PRA）、血浆醛固酮浓度（PAC）和24小时尿醛固酮排泄量。此外，所有受试者均完成了柏林问卷，这是一项旨在识别有睡眠呼吸暂停风险受试者的调查。原发性醛固酮增多症（PA）定义为高尿钠排泄（>200 mEq/24 h）期间PRA<1.0 ng/mL/h且24小时尿醛固酮排泄量>12μg。
根据对柏林问卷的回答，在评估的114名受试者中，72名受试者有睡眠呼吸暂停的高概率，42名受试者有睡眠呼吸暂停的低概率。睡眠呼吸暂停高风险受试者被诊断为PA的可能性几乎是低风险受试者的两倍（36%对19%，p<0.05），PRA往往较低（1.2±1.8 ng/mL/h对1.9±4.1 ng/mL/h），与睡眠呼吸暂停低风险受试者相比，24小时尿醛固酮排泄量显著更高（13.6±9.6μg对9.8±7.6μg，p<0.05）。
这些数据提供了证据，表明患有顽固性高血压和睡眠呼吸暂停症状的受试者醛固酮排泄增加。虽然这种关联的因果关系尚不清楚，但据推测，睡眠呼吸暂停通过刺激醛固酮排泄导致顽固性高血压的发生。
