Obstructive sleep apnea and insight into mechanisms of sympathetic overactivity

J Clin Invest. 2014 Apr;124(4):1454-7. doi: 10.1172/JCI70420. Epub 2014 Apr 1.


Nearly two decades ago, we evaluated ten patients with obstructive sleep apnea (OSA). We determined that alarming nocturnal oscillations in arterial pressure and sympathetic nerve activity (SNA) were caused by regulatory coupling and neural interactions among SNA, apnea, and ventilation. Patients with OSA exhibited high levels of SNA when awake, during normal ventilation, and during normoxia, which contributed to hypertension and organ damage. Additionally, we achieved a beneficial and potentially lifesaving reduction in SNA through the application of continuous positive airway pressure (CPAP), which remains a primary therapeutic approach for patients with OSA. With these results in hindsight, we herein discuss three concepts with functional and therapeutic relevance to the integrative neurobiology of autonomic cardiovascular control and to the mechanisms involved in excessive sympathoexcitation in OSA.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Autonomic Nervous System / physiopathology
  • Blood Pressure / physiology
  • Carotid Body / physiopathology
  • Chemoreceptor Cells / physiology
  • Continuous Positive Airway Pressure
  • Humans
  • Hypertension / physiopathology
  • Neuroimmunomodulation / physiology
  • Neuronal Plasticity / physiology
  • Pressoreceptors / physiopathology
  • Reflex / physiology
  • Sleep Apnea, Obstructive / etiology*
  • Sleep Apnea, Obstructive / physiopathology*
  • Sleep Apnea, Obstructive / therapy
  • Sympathetic Nervous System / physiopathology*