Sympathoexcitation and arterial hypertension associated with obstructive sleep apnea and cyclic intermittent hypoxia.

Abstract

Obstructive sleep apnea (OSA) is characterized by repetitive episodes of upper airway obstruction during sleep. These obstructive episodes are characterized by cyclic intermittent hypoxia (CIH), by sleep fragmentation, and by hemodynamic instability, and they result in sustained sympathoexcitation and elevated arterial pressure that persist during waking, after restoration of normoxia. Early studies established that 1) CIH, rather than sleep disruption, accounts for the increase in arterial pressure; 2) the increase in arterial pressure is a consequence of the sympathoactivation; and 3) arterial hypertension after CIH exposure requires an intact peripheral chemoreflex. More recently, however, evidence has accumulated that sympathoactivation and hypertension after CIH are also dependent on altered central sympathoregulation. Furthermore, although many molecular pathways are activated in both the carotid chemoreceptor and in the central nervous system by CIH exposure, two specific neuromodulators-endothelin-1 and angiotensin II-appear to play crucial roles in mediating the sympathetic and hemodynamic response to intermittent hypoxia.

• Authors: J Woodrow Weiss, Renaud Tamisier, Yuzhen Liu
• Journal: Journal of applied physiology (Bethesda, Md. : 1985) (J Appl Physiol (1985)) Vol. 119 Issue 12 Pg. 1449-54 (Dec 15 2015) ISSN: 1522-1601 [Electronic] United States
• PMID: 26251511 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2015 the American Physiological Society.

Topics

• Animals
• Humans
• Hypertension (epidemiology, etiology, physiopathology)
• Hypoxia (complications, physiopathology)
• Prevalence
• Sleep Apnea, Obstructive (epidemiology, physiopathology)
• Sympathetic Nervous System (physiopathology)