Abnormal vasoactive hormones and 24-hour blood pressure in obstructive sleep apnea

• Published in: American journal of hypertension Vol. 16; no. 4; pp. 274 - 280
• Main Authors: Møller, Dorthe S, Lind, Pernille, Strunge, Benedicte, Pedersen, Erling B
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.04.2003; Oxford University Press; Elsevier Science
• Subjects: 24-h ambulatory blood pressure; Adult; Aged; aldosterone; angiotensin II; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Cardiology. Vascular system; Case-Control Studies; Circadian Rhythm; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; continuous positive airway pressure; Female; Follow-Up Studies; Heart Rate; Hormones - blood; Humans; Hypertension; Male; Medical sciences; Middle Aged; Positive-Pressure Respiration; renin; Sleep Apnea Syndromes - blood; Sleep Apnea Syndromes - physiopathology; Sleep Apnea Syndromes - therapy; Treatment Outcome; Hypertension; 24-h ambulatory blood pressure; continuous positive airway pressure; renin; angiotensin II; aldosterone; Human; Sleep apnea syndrome; Respiratory disease; Enzyme; Pathogenesis; Peptide hormone; Cardiovascular disease; Atrial natriuretic peptide; Aldosterone; Peptidases; Natriuretic hormone; Renin; Risk factor; Hydrolases; Arterial pressure; Aspartic endopeptidases; Ambulatory; Angiotensin II; Monitoring
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/S0895-7061(02)03267-3

Patients with obstructive sleep apnea (OSA) are at increased risk for hypertension. The mechanisms responsible for the development of hypertension are controversial. We hypothesized that patients with OSA had an abnormal 24-h blood pressure (BP) and an abnormal activity in vasoactive hormones, and that both BP and hormones were normalized during treatment with long-term nasal continuous positive airway pressure (CPAP). The 24-h BP and plasma levels of the vasoactive hormones (renin, angiotensin II, aldosterone, atrial natriuretic peptide, brain natriuretic peptide, vasopressin, and endothelin-1) were measured in 24 patients with OSA and in 18 control subjects. Thirteen patients with OSA were reexamined after 14 months of CPAP therapy. Patients with OSA had significantly increased BP and heart rate and a reduced nocturnal BP drop. Both angiotensin II (13.3 ± 1.6 v 7.8 ± 1.0 pmol/L) and aldosterone (94.0 ± 9.4 v 62.2 ± 4.5 pmol/L) were significantly higher in OSA than in control subjects. Positive correlations were found between angiotensin II and daytime BP (systolic: r = 0.49, P < .01; diastolic: r = 0.52, P < .01). The CPAP therapy resulted in a decrease in BP, and this CPAP-induced reduction in BP was correlated with a decrease in both plasma renin ( r = 0.76 to 0.92, all P < .01) and plasma angiotensin II concentration ( r = 0.58 to 0.81, all P < .05). Plasma angiotensin II and aldosterone were elevated in OSA, and plasma angiotensin II was correlated with BP. Long-term CPAP reduced BP, and this decrease in BP was correlated with the reductions in plasma renin and angiotensin II levels. We suggest that OSA mediates hypertension, at least in part, via a stimulation of angiotensin II production.