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

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 Ϯ 2.0 mmHg (mean Ϯ SEM), and eventually produced sustained daytime hypertension to a maximum of 15.7 Ϯ 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. ( J. Clin. Invest. 1997. 99:106-109.)

Spontanous periodic breathing is associated with sympathetic hyperreactivity and baroreceptor dysfunction in hypertension

“…The hypertensive effect of chronic intermittent hypoxia outlasts hypoxemia in animal models. [4,5] Morgan et al demonstrated in healthy volunteers that hypoxic hypercapnia leads to a protracted increase in MSA, whereas hyperoxic hypercapnia only transiently increases sympathetic activity indicating that hypoxemia is responsible for the effect. [40] Chronic intermittent hypoxia has thus clinically relevant prolonged effects on blood pressure in animal models.…”

“…[4] In dogs, hypoxic episodes due to repetitive airway obstruction during sleep resulted in acute transient increases in nighttime blood pressure and eventually provoked a sustained daytime hypertension. [5] It is likely that the same mechanisms are valid in humans too, since obstructive sleep apnea leads to increased SNS activity and increased daytime blood pressure. [6][7][8] Obstructive breathing disorders are associated with cardiovascular diseases such as hypertension, [9][10][11] myocardial infarction, [12] stroke, [13] and heart failure.…”

Inflammation contributes to the atherogenic role of intermittent hypoxia in apolipoprotein-E knock out mice

“…About 60% of OSA-patients develop systemic hypertension 22 , even in the absence of any other risk factors when including both clinical and masked hypertension 4,23 . Using animal models 15,24 and also applying IH in healthy humans 25 suggest that IH is a major factor determining blood pressure increase. We have previously shown in C57BL6 mice that blood pressure surges appear at each hypoxic episode, and are associated with increased sympathetic activation 14 .…”

Predictors of erectile function improvement in obstructive sleep apnea patients with long-term CPAP treatment

“…[4][5][6][7] Their underlying pathological mechanisms include recurrent intermittent hypoxemia and increased sympathetic activity, primarily at the termination of the apneic events. 8,9 In a previous study, 10 our group showed that OSAS is also associated with ED in a dose-related fashion.…”