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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-5-11
pubmed:abstractText
The carotid body plays an important role in initiating protective responses to hypoxemia. The primary oxygen sensing cells are the glomus or type 1 cells. Hypoxia evokes the secretion of neurotransmitters from these cells which then excite afferent nerves. This response is mediated via membrane depolarization and voltage-gated Ca2+ entry. Studies from this laboratory have revealed that membrane depolarization in response to hypoxia is primarily the result of inhibition of background K+ channels which show strong similarities to the acid sensitive tandem-P-domain K+ channels TASK-1 and TASK-3. The background K+ channels of type-1 cells are also very sensitive to inhibition of mitochondrial energy metabolism and, in excised patches, appear to be directly activated by ATP. Thus these TASK-like background channels would appear to confer the ability to sense changes in oxygen levels, pH and metabolism upon the type 1 cell. The key issue of whether the effects of hypoxia are mediated through changes in metabolism remains unanswered but the effects of inhibition of mitochondrial energy metabolism and of hypoxia upon background K+ channels is mutually exclusive suggesting that there is a close link between metabolism and oxygen sensing in the type 1 cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1528-2511
pubmed:author
pubmed:issnType
Print
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-85; discussion 85-94, 131-40
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
The role of TASK-like K+ channels in oxygen sensing in the carotid body.
pubmed:affiliation
University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, UK.
pubmed:publicationType
Journal Article, Review