ArticleRespiratory physiology & neurobiology2011
Role of MaxiK-type calcium dependent K+ channels in rat carotid body hypoxia transduction during postnatal development.
Article in Respiratory physiology & neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Activation of voltage-dependent KThe Journal of physiology · 2018Article
- Increase in cytosolic Ca2+ produced by hypoxia and other depolarizing stimuli activates a non-selective cation channel in chemoreceptor cells of rat carotid body.The Journal of physiology · 2014Article
- Non-additive interactions between mitochondrial complex IV blockers and hypoxia in rat carotid body responses.Respiratory physiology & neurobiology · 2014Article
- K(+) channels in O(2) sensing and postnatal development of carotid body glomus cell response to hypoxia.Respiratory physiology & neurobiology · 2013Review
- Carotid chemoreceptor "resetting" revisited.Respiratory physiology & neurobiology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Carotid body chemoreceptors transduce a decrease in arterial oxygen tension into increased sinus nerve action potential (AP) activity which undergoes a maturational increase in the post-natal period. MaxiK-channels channels are proposed to play a major role in organ function based on their maturation-dependent expression in glomus cells and inhibition by acute hypoxia. To better resolve the role of this channel, single-unit AP activity of rat chemoreceptor neurons was recorded, in vitro, during a progressive decrease in oxygen from normoxia (∼150 Torr) to moderate hypoxia (∼60 Torr). Blockade of MaxiK channels with charybdotoxin (100 nM) in both older (P16-P18) and younger (P2-P3) animals resulted in no significant change in AP activity, but increased nerve conduction speed in the older animals. In dissociated glomus cells, charybdotoxin slightly enhanced the intracellular calcium response to acute hypoxia at both ages. We conclude that MaxiK channels play little or no role in mediating the response to acute, moderate hypoxia, either in the newborn or older animal.
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Registered trials
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