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Cited by 24Neuroscience of respiration and sleepIon channel regulation and functionNeonatal Respiratory Health Research

K+ channels in O2 sensing and postnatal development of carotid body glomus cell response to hypoxia

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Kim, Donghee·2013·Respiratory Physiology & Neurobiology
DOI 10.1016/j.resp.2012.07.005PMC PMC4727403
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Abstract

The sensitivity of carotid body chemoreceptors to hypoxia is low just after birth and increases over the first few weeks of the postnatal period. At present, it is believed that the hypoxia-induced excitation of carotid body glomus cells begins with the inhibition of the outward K(+) current via one or more O(2) sensors. Although the nature of the O(2) sensors and their signals that inhibit the K(+) current are not well defined, studies suggest that the postnatal maturation of the glomus cell response to hypoxia is largely due to the increased sensitivity of K(+) channels to hypoxia. As K(V), BK and TASK channels that are O(2)-sensitive contribute to the K(+) current, it is important to identify the O(2) sensor and the signaling molecule for each of these K(+) channels. Various O(2) sensors (mitochondrial hemeprotein, hemeoxygenase-2, NADPH oxidase) and associated signals have been proposed to mediate the inhibition of K(+) channels by hypoxia. Studies suggest that a mitochondrial hemeprotein is likely to serve as an O(2) sensor for K(+) channels, particularly for TASK, and that multiple signals may be involved. Thus, changes in the sensitivity of the mitochondrial O(2) sensor to hypoxia, the sensitivity of K(+) channels to signals generated by mitochondria, and/or the expression levels of K(+) channels are likely to account for the postnatal maturation of O(2) sensing by glomus cells.

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  • Various K+ channels influenced by hypoxia include voltage-gated K+ channels, Ca2+-activated K+ channels, and ATP-sensitive K+ channels.

    “In the latter, there are various K + channels that are influenced by hypoxia, including voltage-gated K + channels, Ca 2+activated K + channels, and ATP-sensitive K + channels (308, 347).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [308]

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Authors
Kim, D.
Affiliations
Rosalind Franklin University of Medicine and Science (US)
Corresponding author
Kim, Donghee
ORCID
Kim, Donghee
Venue
Respiratory Physiology & Neurobiology
Publisher
Elsevier BV
Published
2013-01
Volume
185
Issue
1
Pages
44-56
ISSN
1569-9048 (ISSN-L)
DOI
10.1016/j.resp.2012.07.005
PMC
PMC4727403
OpenAlex
W2016315253
Cited by
24
References
92
Citations by year
2026: 2 · 2024: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 2 · 2014: 2 · 2013: 2 · 2012: 2
FWCI
0.29
Type
journal article
Language
en
Open access
Licence
Locations
  • Respiratory Physiology & Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01hl054621-12)
  • National Heart, Lung, and Blood Institute (R01HL111497, R01 HL-054621)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
Keywords
oxygen sensing, carotid body, glomus cells, hypoxia, potassium channels, postnatal development, TASK channels, BK channels, voltage-gated potassium channels, NADPH oxidase
MeSH terms
Animals, Carotid Body, Humans, Oxygen, Potassium Channels

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