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3 ALDOSTERONE EXCRETION IS NOT RELATED TO SLEEP DISRUPTION IN SUBJECTS WITH RESISTANT HYPERTENSION.
  1. A. E. Thomas,
  2. M. N. Pratt-Ubunama,
  3. S. M. Harding,
  4. D. A. Calhoun
  1. Department of Vascular Biology, University of Alabama at Birmingham, Birmingham, AL

Abstract

Introduction Studies indicate a strong association between obstructive sleep apnea (OSA) and hypertension, particularly in subjects with resistant hypertension. We have previously reported that aldosterone excretion is related to severity of OSA in subjects with resistant hypertension leading us to hypothesize that intermittent hypoxemia associated with OSA stimulates aldosterone release. In the current study, we tested the alternative hypothesis that sleep disruption is related to aldosterone excretion in subjects with resistant hypertension.

Methods Subjects referred to UAB for resistant hypertension were evaluated for urinary aldosterone (24-hour) and plasma aldosterone. Subjects were also evaluated by full-night polysomnography. The apnea-hypopnea index (AHI), hypoxic index (HI), and nonrespiratory arousal index were quantified and related to aldosterone excretion.

Results A total of 74 subjects were evaluated. The subjects were on an average of 4.0 6 1.2 antihypertensive medications and the mean blood pressure was 156 6 27/89 6 14 mm Hg. The mean AHI was 25.8 6 25 events per hour. The AHI was correlated with urinary aldosterone (r = .55, p < .0001) and plasma aldosterone (r = .54, p < .0001). Similarly, the mean HI was 7.5 6 10.5 and was correlated with urinary aldosterone (r = .41, p = .0004) and plasma aldosterone (r = .51, p < .0001). The mean nonrespiratory arousal index was 5.1 6 5.6 events per hour. The nonrespiratory arousal index was not related to urinary or plasma aldosterone levels (r = .09, p = .44; r = .08, p = .54, respectively).

Conclusion These data demonstrate that the relation between aldosterone excretion and severity of OSA in subjects with resistant hypertension is not explained by sleep disruption, ie, nonrespiratory arousal index. These results support our original hypothesis that the intermittent hypoxemia associated with OSA is the stimulus of OSA-induced aldosterone excretion.

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