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Carotid body type-I cells under chronic sustained hypoxia: Focus on metabolism and membrane excitability

dc.contributor.authorPulgar-Sepúlveda R.
dc.contributor.authorVaras R.
dc.contributor.authorIturriaga R.
dc.contributor.authorDel Rio R.
dc.contributor.authorOrtiz F.C.
dc.date.accessioned2020-09-02T22:25:59Z
dc.date.available2020-09-02T22:25:59Z
dc.date.issued2018
dc.identifier10.3389/fphys.2018.01282
dc.identifier.citation9, SEP, -
dc.identifier.issn1664042X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5858
dc.descriptionChronic sustained hypoxia (CSH) evokes ventilatory acclimatization characterized by a progressive hyperventilation due to a potentiation of the carotid body (CB) chemosensory response to hypoxia. The transduction of the hypoxic stimulus in the CB begins with the inhibition of K+ currents in the chemosensory (type-I) cells, which in turn leads to membrane depolarization, Ca2+ entry and the subsequent release of one- or more-excitatory neurotransmitters. Several studies have shown that CSH modifies both the level of transmitters and chemoreceptor cell metabolism within the CB. Most of these studies have been focused on the role played by such putative transmitters and modulators of CB chemoreception, but less is known about the effect of CSH on metabolism and membrane excitability of type-I cells. In this mini-review, we will examine the effects of CSH on the ion channels activity and excitability of type-I cell, with a particular focus on the effects of CSH on the TASK-like background K+ channel. We propose that changes on TASK-like channel activity induced by CSH may contribute to explain the potentiation of CB chemosensory activity. Copyright © 2018 Pulgar-Sepúlveda, Varas, Iturriaga, Del Rio and Ortiz.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectCarotid body
dc.subjectChronic hypoxia
dc.subjectIon channels
dc.subjectMembrane depolarization
dc.subjectTASK-like channel
dc.subjectadenosine triphosphate
dc.subjectcalcium ion
dc.subjectchloride channel
dc.subjectcholinergic receptor
dc.subjectdopamine
dc.subjectendothelin 1
dc.subjectheme oxygenase 2
dc.subjecthypoxia inducible factor
dc.subjecthypoxia inducible factor 1beta
dc.subjecthypoxia inducible factor 2alpha
dc.subjectneurotransmitter
dc.subjectnitric oxide
dc.subjectpotassium ion
dc.subjectsodium ion
dc.subjectvoltage gated calcium channel
dc.subjectcarotid body chemoreceptor
dc.subjectcarotid body type I cell
dc.subjectcell activation
dc.subjectcell function
dc.subjectcell hypoxia
dc.subjectcell metabolism
dc.subjectcell proliferation
dc.subjectchemoreceptor cell
dc.subjectchronic sustained hypoxia
dc.subjectconductance
dc.subjecthuman
dc.subjectintracellular membrane
dc.subjectmembrane depolarization
dc.subjectmembrane potential
dc.subjectnerve cell excitability
dc.subjectneurotransmission
dc.subjectnonhuman
dc.subjectosmolarity
dc.subjectoxidative phosphorylation
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein secretion
dc.subjectReview
dc.subjectsensitization
dc.titleCarotid body type-I cells under chronic sustained hypoxia: Focus on metabolism and membrane excitability
dc.typeReview


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