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Conference Paper: Nitric oxide deficit is part of the maladaptive paracrine-autocrine response of the carotid body to intermittent hypoxia in sleep apnea

TitleNitric oxide deficit is part of the maladaptive paracrine-autocrine response of the carotid body to intermittent hypoxia in sleep apnea
Authors
KeywordsChemoreceptor
NO synthase
Obstructive sleep apnea
Issue Date2015
PublisherSpringer International Publishing.
Citation
The 19th International Meeting of the International Society for Arterial Chemoreception (ISAC-19), Leeds, UK., 29 June-3 July 2014. In Advances in Experimental Medicine and Biology, 2015, v. 860, p. 233-237. How to Cite?
AbstractThe carotid body functions to maintain the blood gas homeostasis, whereas anomalous carotid chemoreceptor activities could be pathogenic in patients with sleep apnea. Recent findings suggest an upregulation of renin-angiotensin system (Lam SY, Liu Y, Ng KM et al. Exp Physiol 99:220–231, 2014), which could lead to inflammation in the carotid body during intermittent hypoxia (Lam SY, Liu Y, Ng KM et al. Histochem Cell Biol 137:303–317, 2012). In addition, the level of nitric oxide detected in the carotid body was significantly decreased following intermittent hypoxia for days. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body, which could play a role in the pathophysiological cascade of sleep apnea in patients with an overactivity of the chemoreflex.
DescriptionAdv Exp Med Biol v.860 entitled: Arterial Chemoreceptors in Physiology and Pathophysiology
Persistent Identifierhttp://hdl.handle.net/10722/231448
ISBN
ISSN
2015 Impact Factor: 1.953
2015 SCImago Journal Rankings: 0.887

 

DC FieldValueLanguage
dc.contributor.authorFung, ML-
dc.date.accessioned2016-09-20T05:23:11Z-
dc.date.available2016-09-20T05:23:11Z-
dc.date.issued2015-
dc.identifier.citationThe 19th International Meeting of the International Society for Arterial Chemoreception (ISAC-19), Leeds, UK., 29 June-3 July 2014. In Advances in Experimental Medicine and Biology, 2015, v. 860, p. 233-237.-
dc.identifier.isbn978-3-319-18439-5-
dc.identifier.issn0065-2598-
dc.identifier.urihttp://hdl.handle.net/10722/231448-
dc.descriptionAdv Exp Med Biol v.860 entitled: Arterial Chemoreceptors in Physiology and Pathophysiology-
dc.description.abstractThe carotid body functions to maintain the blood gas homeostasis, whereas anomalous carotid chemoreceptor activities could be pathogenic in patients with sleep apnea. Recent findings suggest an upregulation of renin-angiotensin system (Lam SY, Liu Y, Ng KM et al. Exp Physiol 99:220–231, 2014), which could lead to inflammation in the carotid body during intermittent hypoxia (Lam SY, Liu Y, Ng KM et al. Histochem Cell Biol 137:303–317, 2012). In addition, the level of nitric oxide detected in the carotid body was significantly decreased following intermittent hypoxia for days. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body, which could play a role in the pathophysiological cascade of sleep apnea in patients with an overactivity of the chemoreflex.-
dc.languageeng-
dc.publisherSpringer International Publishing.-
dc.relation.ispartofAdvances in Experimental Medicine and Biology-
dc.relation.ispartofArterial Chemoreceptors in Physiology and Pathophysiology-
dc.subjectChemoreceptor-
dc.subjectNO synthase-
dc.subjectObstructive sleep apnea-
dc.titleNitric oxide deficit is part of the maladaptive paracrine-autocrine response of the carotid body to intermittent hypoxia in sleep apnea-
dc.typeConference_Paper-
dc.identifier.emailFung, ML: fungml@hku.hk-
dc.identifier.authorityFung, ML=rp00433-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1007/978-3-319-18440-1_26-
dc.identifier.pmid26303486-
dc.identifier.scopuseid_2-s2.0-84940122046-
dc.identifier.hkuros266077-
dc.identifier.hkuros252249-
dc.identifier.spage233-
dc.identifier.epage237-
dc.publisher.placeSwitzerland-
dc.customcontrol.immutablesml 170504 amended-

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