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: 92/1/39    most recent expphysiol.2006.036434v1 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 Google Scholar Google Scholar Articles by Prabhakar, N. R. Articles by Kumar, G. K. Search for Related Content PubMed PubMed Citation Articles by Prabhakar, N. R. Articles by Kumar, G. K. Related Collections Themed Issue papers

Departments of ¹ Physiology & Biophysics² Medicine³ Pathology⁴ Biochemistry, Case Western School of Medicine, Cleveland, OH, USA

Patients with recurrent apnoeas exhibit autonomic abnormalities manifested as persistent increase in sympathetic nerve activity (SNA). Several studies suggest that chronic intermittent hypoxia (CIH) resulting from recurrent apnoeas is a major stimulus for evoking autonomic morbidity. Although it has been proposed that CIH, by way of activating the chemoreceptor reflex, leads to sympathetic excitation, the underlying mechanisms are incompletely understood. Studies on experimental models have provided new insights into the mechanisms associated with CIH-evoked sympathoexcitation. The purpose of this article is to highlight recent information on systemic, cellular and molecular analysis of the effects of CIH on chemoreceptor-mediated sympathoexcitation. Chronic intermittent hypoxia exerts two major effects on the chemoreceptor reflex: (a) augmentation of the carotid body and sympathetic effector responses to acute hypoxia; and (b) induction of long-lasting activation of both the sensor and the effector that persists several hours after termination of CIH. Available evidence indicates that CIH may facilitate processing of chemoreceptor afferent information at the central nervous system. Recent studies suggest that reactive oxygen species-mediated signalling is a major cellular mechanism, and transcriptional activation by hypoxia-inducible factor-1 is one of the critical molecular mechanisms underlying chemoreceptor-mediated sympathoexcitation by CIH.

(Received 3 November 2006; accepted after revision 6 November 2006; first published online 23 November 2006)
Corresponding author N. R. Prabhakar: Department of Physiology & Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44109, USA. Email: nrp{at}case.edu