ReviewRespiratory physiology & neurobiology2013
K(+) channels in O(2) sensing and postnatal development of carotid body glomus cell response to hypoxia.
Review in Respiratory physiology & neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Acute Hypoxia Inhibits KActa physiologica (Oxford, England) · 2026Article
- Hypoxic Signaling Pathways in Carotid Body Tumors.Cancers · 2024Review
- Genetic variants in eleven central and peripheral chemoreceptor genes in sudden infant death syndrome.Pediatric research · 2022Article
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms.The Journal of physiology · 2018Review
- Placental Origins of Chronic Disease.Physiological reviews · 2016Review
- THIK-1 (K2P13.1) is a small-conductance background K(+) channel in rat trigeminal ganglion neurons.Pflugers Archiv : European journal of physiology · 2014Article
- 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
- Effects of modulators of AMP-activated protein kinase on TASK-1/3 and intracellular Ca(2+) concentration in rat carotid body glomus cells.Respiratory physiology & neurobiology · 2014Article
- Acute Hypoxia Activates an ENaC-like Channel in Rat Pheochromocytoma (PC12) Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
- Carotid chemoreceptor "resetting" revisited.Respiratory physiology & neurobiology · 2013Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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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