File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Mechanisms of maladaptive responses of peripheral chemoreceptors to intermittent hypoxia in sleep-disordered breathing

TitleMechanisms of maladaptive responses of peripheral chemoreceptors to intermittent hypoxia in sleep-disordered breathing
Authors
Issue Date2014
PublisherScience Press. The Journal's web site is located at http://www.actaps.com.cn
Citation
Acta Physiologica Sinica, 2014, v. 66 n. 1, p. 23-29 How to Cite?
AbstractPeripheral chemoreceptors in the carotid body play important roles in the transduction of chemical stimuli in the arterial blood to the central for eliciting the chemoreflex, which mediates the ventilatory and circulatory responses to hypoxia. The activity of carotid chemoreceptor is modulated and significantly contributes to the ventilatory acclimatization at high altitude. In addition, the carotid chemoreceptor activity is augmented in patients with sleep-disordered breathing, notably in central or obstructive sleep apnea, and also in experimental animals. Thus, the carotid body functions to maintain the oxygen homeostasis, whereas anomalous carotid chemoreceptor activities could be both adaptive and pathogenic in sleep apnea. This review aims to summarize the cellular and molecular mechanisms that could mediate the augmented chemoreceptor activity induced by intermittent hypoxia. Our recent findings suggest a pathogenic role of inflammation mediated by an upregulation of renin-angiotensin system in the carotid body in the over-activity of the chemoreflex. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body function, which could play a role in the pathophysiology of sleep apnea.
Persistent Identifierhttp://hdl.handle.net/10722/255674
ISSN
2015 SCImago Journal Rankings: 0.240

 

DC FieldValueLanguage
dc.contributor.authorFung, ML-
dc.contributor.authorTipoe, GL-
dc.contributor.authorLeung, PS-
dc.date.accessioned2018-07-11T07:07:02Z-
dc.date.available2018-07-11T07:07:02Z-
dc.date.issued2014-
dc.identifier.citationActa Physiologica Sinica, 2014, v. 66 n. 1, p. 23-29-
dc.identifier.issn0371-0874-
dc.identifier.urihttp://hdl.handle.net/10722/255674-
dc.description.abstractPeripheral chemoreceptors in the carotid body play important roles in the transduction of chemical stimuli in the arterial blood to the central for eliciting the chemoreflex, which mediates the ventilatory and circulatory responses to hypoxia. The activity of carotid chemoreceptor is modulated and significantly contributes to the ventilatory acclimatization at high altitude. In addition, the carotid chemoreceptor activity is augmented in patients with sleep-disordered breathing, notably in central or obstructive sleep apnea, and also in experimental animals. Thus, the carotid body functions to maintain the oxygen homeostasis, whereas anomalous carotid chemoreceptor activities could be both adaptive and pathogenic in sleep apnea. This review aims to summarize the cellular and molecular mechanisms that could mediate the augmented chemoreceptor activity induced by intermittent hypoxia. Our recent findings suggest a pathogenic role of inflammation mediated by an upregulation of renin-angiotensin system in the carotid body in the over-activity of the chemoreflex. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body function, which could play a role in the pathophysiology of sleep apnea.-
dc.languageeng-
dc.publisherScience Press. The Journal's web site is located at http://www.actaps.com.cn-
dc.relation.ispartofActa Physiologica Sinica-
dc.titleMechanisms of maladaptive responses of peripheral chemoreceptors to intermittent hypoxia in sleep-disordered breathing-
dc.typeArticle-
dc.identifier.emailFung, ML: fungml@hkucc.hku.hk-
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.identifier.authorityTipoe, GL=rp00371-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid24553866-
dc.identifier.hkuros238109-
dc.identifier.volume66-
dc.identifier.issue1-
dc.identifier.spage23-
dc.identifier.epage29-
dc.publisher.placeChina-
dc.identifier.issnl0371-0874-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats