Aldosterone excretion among subjects with resistant hypertension and symptoms of sleep apnea
Aldosterone excretion among subjects with resistant hypertension and symptoms of sleep apnea
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DOI：
10.1378/chest.125.1.112
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发表时间：
2004-01-01
期刊：
影响因子：
9.6
通讯作者：
Harding, SM
中科院分区：
文献类型：
--
作者：
Calhoun, DA;Nishizaka, MK;Harding, SM
目的：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的机制尚不清楚。观察到原发性醛固酮增多症高血压患者中OSA的高患病率，我们假设睡眠呼吸暂停与醛固酮排泄之间可能存在关联。设计：在一所大学诊所的顽固性高血压患者中，我们前瞻性地测定了高盐摄入期间血浆肾素活性（PRA）、血浆醛固酮浓度（PAC）和24小时尿醛固酮排泄量。此外，所有受试者都完成了柏林问卷调查，这是一项旨在确定有睡眠呼吸暂停风险的受试者的调查。原发性醛固酮增多症（PA）定义为PRA < 1.0 ng/mL/h， 24小时尿醛固酮排泄，高尿钠排泄（> 200 mEq/24 h）期间> 12杯。结果：在114名受试者中，根据他们对柏林问卷的回答，72名受试者有高概率睡眠呼吸暂停，42名受试者有低概率睡眠呼吸暂停。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% vs 19%, p < 0.05）， PRA倾向于较低（1.2 +/- 1.8 ng/mL/h vs 1.9 +/- 4.1 ng/mL/h）， 24小时尿醛固酮排泄量显著高于低风险睡眠呼吸暂停受试者（13.6 +/- 9.6马克vs 9.8 +/- 7.6马克，p < 0.05）。结论：这些数据为顽固性高血压和睡眠呼吸暂停症状患者醛固酮分泌增加提供了证据。虽然这种关联的因果关系尚不清楚，但假设睡眠呼吸暂停通过刺激醛固酮的分泌来促进顽固性高血压的发展。
Objective: 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.Design: 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 mug during high urinary sodium excretion (> 200 mEq/24 h).Results: Of the 114 subjects evaluated, 72 subjects had a high probability and 42 subjects bad 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 mug vs 9.8 +/- 7.6 mug, p < 0.05) compared to subjects at low risk of sleep apnea.Conclusion: 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.