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Enhanced carotid body chemosensory activity and the cardiovascular alterations induced by intermittent hypoxia
dc.contributor.author | Iturriaga R. | |
dc.contributor.author | Andrade D.C. | |
dc.contributor.author | Del Rio R. | |
dc.date.accessioned | 2020-09-02T22:20:40Z | |
dc.date.available | 2020-09-02T22:20:40Z | |
dc.date.issued | 2014 | |
dc.identifier | 10.3389/fphys.2014.00468 | |
dc.identifier.citation | 5, Nov, - | |
dc.identifier.issn | 1664042X | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4956 | |
dc.description | The carotid body (CB) plays a main role in the maintenance of the oxygen homeostasis. The hypoxic stimulation of the CB increases the chemosensory discharge, which in turn elicits reflex sympathetic, cardiovascular and ventilatory adjustments. An exacerbate carotid chemosensory activity has been associated with human sympathetic-mediated diseases such as hypertension, insulin resistance, heart failure and obstructive sleep apnea (OSA). Indeed, the CB chemosensory discharge becomes tonically hypereactive in experimental models of OSA and heart failure. Chronic intermittent hypoxia (CIH), a main feature of OSA, enhances CB chemosensory baseline discharges in normoxia and in response to hypoxia, inducing sympathetic overactivity and hypertension. Oxidative stress, increased levels of ET-1, Angiotensin II and pro-inflammatory cytokines, along with a reduced production of NO in the CB, have been associated with the enhanced carotid chemosensory activity. In this review, we will discuss new evidence supporting a main role for the CB chemoreceptor in the autonomic and cardiorespiratory alterations induced by intermittent hypoxia, as well as the molecular mechanisms involved in the CB chemosensory potentiation. © 2014 Iturriaga, Andrade and Del_rio. | |
dc.language.iso | en | |
dc.publisher | Frontiers Media S.A. | |
dc.subject | Autonomic dysfunction | |
dc.subject | Carotid body | |
dc.subject | Hypertension | |
dc.subject | Intermittent hypoxia | |
dc.subject | Oxidative stress | |
dc.subject | angiotensin II | |
dc.subject | bosentan | |
dc.subject | cyclo(dextro tryptophyl dextro aspartylprolyl dextro valylleucyl) | |
dc.subject | cytokine | |
dc.subject | endothelin 1 | |
dc.subject | hypoxia inducible factor 1alpha | |
dc.subject | immunoglobulin enhancer binding protein | |
dc.subject | interleukin 1beta | |
dc.subject | interleukin 6 | |
dc.subject | nitric oxide | |
dc.subject | noradrenalin | |
dc.subject | reactive nitrogen species | |
dc.subject | reactive oxygen metabolite | |
dc.subject | reduced nicotinamide adenine dinucleotide phosphate oxidase 2 | |
dc.subject | tempol | |
dc.subject | transcription factor NFAT3 | |
dc.subject | tumor necrosis factor alpha | |
dc.subject | autonomic dysfunction | |
dc.subject | cardiovascular disease | |
dc.subject | carotid body chemoreceptor | |
dc.subject | chronic intermittent hypoxia | |
dc.subject | clinical feature | |
dc.subject | disease association | |
dc.subject | disease classification | |
dc.subject | disease course | |
dc.subject | disease severity | |
dc.subject | endothelial dysfunction | |
dc.subject | enzyme activation | |
dc.subject | human | |
dc.subject | hyperactivity | |
dc.subject | hypertension | |
dc.subject | immunoreactivity | |
dc.subject | inflammation | |
dc.subject | molecular mechanics | |
dc.subject | nonhuman | |
dc.subject | oxidative stress | |
dc.subject | pathophysiology | |
dc.subject | protein expression | |
dc.subject | protein function | |
dc.subject | protein synthesis | |
dc.subject | renin angiotensin aldosterone system | |
dc.subject | Review | |
dc.subject | risk factor | |
dc.subject | sleep disordered breathing | |
dc.subject | upregulation | |
dc.title | Enhanced carotid body chemosensory activity and the cardiovascular alterations induced by intermittent hypoxia | |
dc.type | Review |