Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model.

TLDR

Epidemiological studies link OSA to systemic hypertension, yet a definitive causal relationship and underlying mechanisms remain unproven. This study aimed to systematically assess how OSA influences daytime and nighttime blood pressure. Four dogs were subjected to intermittent airway occlusion during sleep to induce OSA, and their BP was monitored before, during, and after 1–3 months of exposure. OSA produced transient nighttime BP surges up to 13 mmHg and ultimately sustained daytime hypertension reaching 15.7 mmHg, whereas arousal without occlusion did not elevate BP, confirming OSA can cause persistent hypertension.

Abstract

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.