Advertisement
Research Article Free access | 10.1172/JCI119120
Department of Medicine, University of Toronto, Ontario, Canada.
Find articles by Brooks, D. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Toronto, Ontario, Canada.
Find articles by Horner, R. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Toronto, Ontario, Canada.
Find articles by Kozar, L. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Toronto, Ontario, Canada.
Find articles by Render-Teixeira, C. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Toronto, Ontario, Canada.
Find articles by Phillipson, E. in: JCI | PubMed | Google Scholar
Published January 1, 1997 - More info
Several epidemiological studies have identified obstructive sleep apnea (OSA) as a risk factor for systemic hypertension, but a direct etiologic link between the two disorders has not been established definitively. Furthermore, the specific physiological mechanisms underlying the association between OSA and systemic hypertension have not been identified. The purpose of this study was to systematically examine the effects of OSA on daytime and nighttime blood pressure (BP). We induced OSA in four dogs by intermittent airway occlusion during nocturnal sleep. Daytime and nighttime BP were measured before, during, and after a 1-3-mo long period of OSA. OSA resulted in acute transient increases in nighttime BP to a maximum of 13.0+/-2.0 mmHg (mean+/-SEM), and eventually produced sustained daytime hypertension to a maximum of 15.7+/-4.3 mmHg. In a subsequent protocol, recurrent arousal from sleep without airway occlusion did not result in daytime hypertension. The demonstration that OSA can lead to the development of sustained hypertension has considerable importance, given the high prevalence of both disorders in the population.