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Aldosterone Excretion Among Subjects With Resistant Hypertension and Symptoms of Sleep Apnea^*

^* From the Vascular Biology and Hypertension Program, Division of Cardiovascular Disease (Drs. Nishizaka and Zaman), Veterans Affairs Medical Center (Dr. Calhoun), and the UAB Sleep/Wake Disorders Center, Division of Pulmonary, Allergy and Critical Care Medicine (Dr. Harding), University of Alabama at Birmingham, Birmingham, AL.

Correspondence to: David A. Calhoun, MD, 520 ZRB, 703 South Nineteenth St, Birmingham, AL 35294-0007; e-mail: dcalhoun{at}uab.edu

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 µg during high urinary sodium excretion (> 200 mEq/24 h).

Results: 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 µg vs 9.8 ± 7.6 µg, 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.

Key Words: hyperaldosteronism • hypertension • renin • sleep apnea

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