HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/51    most recent expphysiol.2006.035204v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Foster, G. E. Articles by Hanly, P. J. Search for Related Content PubMed PubMed Citation Articles by Foster, G. E. Articles by Hanly, P. J. Related Collections Themed Issue papers

Departments of ¹ Physiology and Biophysics² Medicine³ Clinical Neurosciences, Faculty of Medicine⁴ Faculty of Kinesiology, University of Calgary, Heritage Medical Research Building, 3330 Hospital Drive NW, Calgary, Alberta, Canada, T2N 4N1

Obstructive sleep apnoea (OSA) has been implicated as a risk factor for the development of hypertension, stroke and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflammation, atherosclerosis, endothelial dysfunction and hypertension. These proposed mechanisms have been drawn from basic research in animal and human models of intermittent hypoxia in addition to clinical investigation of patients with OSA. This review outlines the association between OSA and vascular disease, describes basic mechanisms that may be responsible for this association and compares the results from studies of OSA subjects with those in experimental models of intermittent hypoxia.

(Received 5 September 2006; accepted after revision 15 November 2006; first published online 23 November 2006)
Corresponding author P. J. Hanly: Department of Medicine, Faculty of Medicine, University of Calgary, Health Sciences Center, Room 1421, 3330 Hospital Drive NW, Calgary, Alberta, Canada, T2N 4N1. Email: phanly{at}ucalgary.ca

This article has been cited by other articles:

				J. Aittokallio, O. Polo, J. Hiissa, A. Virkki, J. Toikka, O. Raitakari, T. Saaresranta, and T. Aittokallio Overnight variability in transcutaneous carbon dioxide predicts vascular impairment in women Exp Physiol, July 1, 2008; 93(7): 880 - 891. [Abstract] [Full Text] [PDF]

				T. V. Serebrovskaya, E. B. Manukhina, M. L. Smith, H. F. Downey, and R. T. Mallet Intermittent Hypoxia: Cause of or Therapy for Systemic Hypertension? Experimental Biology and Medicine, June 1, 2008; 233(6): 627 - 650. [Abstract] [Full Text] [PDF]

				M. A. Robinson, J. E. Baumgardner, V. P. Good, and C. M. Otto Physiological and hypoxic O2 tensions rapidly regulate NO production by stimulated macrophages Am J Physiol Cell Physiol, April 1, 2008; 294(4): C1079 - C1087. [Abstract] [Full Text] [PDF]

				E. Tasali and M. S. M. Ip Obstructive Sleep Apnea and Metabolic Syndrome: Alterations in Glucose Metabolism and Inflammation Proceedings of the ATS, February 15, 2008; 5(2): 207 - 217. [Abstract] [Full Text] [PDF]

				V. Ivancev, I. Palada, Z. Valic, A. Obad, D. Bakovic, N. M. Dietz, M. J. Joyner, and Z. Dujic Cerebrovascular reactivity to hypercapnia is unimpaired in breath-hold divers J. Physiol., July 15, 2007; 582(2): 723 - 730. [Abstract] [Full Text] [PDF]

				M. L. Smith Sleep Apnoea and Hypertension: Physiological Bases for a Causal Relation Themed Issue Exp Physiol, January 1, 2007; 92(1): 19 - 20. [Full Text] [PDF]

				M. L. Smith and C. F. Pacchia Sleep Apnoea & Hypertension: Physiological bases for a causal relation: Sleep apnoea and hypertension: role of chemoreflexes in humans Exp Physiol, January 1, 2007; 92(1): 45 - 50. [Abstract] [Full Text] [PDF]