Sympathetic nerve activity in obstructive sleep apnoea
Article first published online: 28 FEB 2003
Acta Physiologica Scandinavica
Volume 177, Issue 3, pages 385–390, March 2003
How to Cite
Narkiewicz, K. and Somers, V. K. (2003), Sympathetic nerve activity in obstructive sleep apnoea. Acta Physiologica Scandinavica, 177: 385–390. doi: 10.1046/j.1365-201X.2003.01091.x
- Issue published online: 28 FEB 2003
- Article first published online: 28 FEB 2003
- Received 1 November 2002, accepted 15 December 2002
- autonomic nervous system;
- blood pressure;
- heart rate;
- sleep apnoea;
- sympathetic nervous system.
The mechanisms underlying the link between obstructive sleep apnoea (OSA) and cardiovascular disease are not completely established. However, there is increasing evidence that autonomic mechanisms are implicated. A number of studies have consistently shown that patients with OSA have high levels of sympathetic nerve traffic. During sleep, repetitive episodes of hypoxia, hypercapnia and obstructive apnoea act through chemoreceptor reflexes and other mechanisms to increase sympathetic drive. Remarkably, the high sympathetic drive is present even during daytime wakefulness when subjects are breathing normally and no evidence of hypoxia or chemoreflex activation is apparent. Several neural and humoral mechanisms may contribute to maintenance of higher sympathetic activity and blood pressure. These mechanisms include chemoreflex and baroreflex dysfunction, altered cardiovascular variability, vasoconstrictor effects of nocturnal endothelin release and endothelial dysfunction. Long-term continuous positive airway pressure treatment decreases muscle sympathetic nerve activity in OSA patients. The vast majority of OSA patients remain undiagnosed. Unrecognized OSA may contribute, in part, to the metabolic and cardiovascular derangements that are thought to be linked to obesity, and to the association between obesity and cardiovascular risk. Furthermore, acting through sympathetic neural mechanisms, OSA may contribute to or augment elevated levels of blood pressure in a large proportion of the hypertensive patient population.