Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
1640339
Reference Type
Journal Article
Subtype
Review
Title
Cellular mechanisms of oxygen sensing at the carotid body: heme proteins and ion channels
Author(s)
Prabhakar, NR; Overholt, JL
Year
2000
Is Peer Reviewed?
1
Journal
Respiration Physiology
ISSN:
0034-5687
Volume
122
Issue
2-3
Page Numbers
209-221
Language
English
PMID
10967345
Web of Science Id
WOS:000089116600010
Abstract
The purpose of this article is to highlight some recent concepts on oxygen sensing mechanisms at the carotid body chemoreceptors. Most available evidence suggests that glomus (type I) cells are the initial site of transduction and they release transmitters in response to hypoxia, which in turn depolarize the nearby afferent nerve ending, leading to an increase in sensory discharge. Two main hypotheses have been advanced to explain the initiation of the transduction process that triggers transmitter release. One hypothesis assumes that a biochemical event associated with a heme protein triggers the transduction cascade. Supporting this idea it has been shown that hypoxia affects mitochondrial cytochromes. In addition, there is a body of evidence implicating non-mitochondrial enzymes such as NADPH oxidases, NO synthases and heme oxygenases located in glomus cells. These proteins could contribute to transduction via generation of reactive oxygen species, nitric oxide and/or carbon monoxide. The other hypothesis suggests that a K(+) channel protein is the oxygen sensor and inhibition of this channel and the ensuing depolarization is the initial event in transduction. Several oxygen sensitive K(+) channels have been identified. However, their roles in initiation of the transduction cascade and/or cell excitability are unclear. In addition, recent studies indicate that molecular oxygen and a variety of neurotransmitters may also modulate Ca(2+) channels. Most importantly, it is possible that the carotid body response to oxygen requires multiple sensors, and they work together to shape the overall sensory response of the carotid body over a wide range of arterial oxygen tensions.
Keywords
carotid body; O2 sensing; ion channels; K+; oxygen; reactive species; transduction; carotid body
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity