ArticleThe Journal of biological chemistry2007
AMP-activated protein kinase mediates carotid body excitation by hypoxia.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 150 citations in OpenAlex.
- AMPK-mediated HCN4 channel phosphorylation contributes to age-related intrinsic bradycardia.The Journal of general physiology · 2026Article
- Chronic Metformin Administration Does Not Alter Carotid Sinus Nerve Activity in Control Rats.Advances in experimental medicine and biology · 2023Article
- Compartmentalization, a key mechanism controlling the multitasking role of the SnRK1 complex.Journal of experimental botany · 2022Review
- Are Multiple Mitochondrial Related Signalling Pathways Involved in Carotid Body Oxygen Sensing?Frontiers in physiology · 2022Review
- Chemoreflex Control as the Cornerstone in Immersion Water Sports: Possible Role on Breath-Hold.Frontiers in physiology · 2022Review
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Activation of AMPK under Hypoxia: Many Roads Leading to Rome.International journal of molecular sciences · 2020Review
- Brain Glucose-Sensing Mechanism and Energy Homeostasis.Molecular neurobiology · 2019Review
- AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018Review
- Ecto-5'-nucleotidase (CD73) regulates peripheral chemoreceptor activity and cardiorespiratory responses to hypoxia.The Journal of physiology · 2018Article
- Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms.The Journal of physiology · 2018Review
- Involvement of AMP-activated Protein Kinase (AMPK) in Regulation of Cell Membrane Potential in a Gastric Cancer Cell Line.Scientific reports · 2018Article
- Carotid Body Type-I Cells Under Chronic Sustained Hypoxia: Focus on Metabolism and Membrane Excitability.Frontiers in physiology · 2018Article
- Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals.Frontiers in physiology · 2018Review
- Is Carotid Body Physiological OFrontiers in physiology · 2018Review
- Oxidative phosphorylation: regulation and role in cellular and tissue metabolism.The Journal of physiology · 2017Review
- Mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone induces vasorelaxation without involving KBritish journal of pharmacology · 2016Article
- The emerging role of AMPK in the regulation of breathing and oxygen supply.The Biochemical journal · 2016Review
- Single cell transcriptome analysis of mouse carotid body glomus cells.The Journal of physiology · 2016Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Early detection of an O2 deficit in the bloodstream is essential to initiate corrective changes in the breathing pattern of mammals. Carotid bodies serve an essential role in this respect; their type I cells depolarize when O2 levels fall, causing voltage-gated Ca2+ entry. Subsequent neurosecretion elicits increased afferent chemosensory fiber discharge to induce appropriate changes in respiratory function (1). Although depolarization of type I cells by hypoxia is known to arise from K+ channel inhibition, the identity of the signaling pathway has been contested, and the coupling mechanism is unknown (2). We tested the hypothesis that AMP-activated protein kinase (AMPK) is the effector of hypoxic chemotransduction. AMPK is co-localized at the plasma membrane of type I cells with O2-sensitive K+ channels. In isolated type I cells, activation of AMPK using 5-aminoimidazole-4-carboxamide riboside (AICAR) inhibited O2-sensitive K+ currents (carried by large conductance Ca2+-activated (BKCa) channels and TASK (tandem pore, acid-sensing potassium channel)-like channels, leading to plasma membrane depolarization, Ca2+ influx, and increased chemosensory fiber discharge. Conversely, the AMPK antagonist compound C reversed the effects of hypoxia and AICAR on type I cell and carotid body activation. These results suggest that AMPK activation is both sufficient and necessary for the effects of hypoxia. Furthermore, AMPK activation inhibited currents carried by recombinant BKCa channels, whereas purified AMPK phosphorylated thealpha subunit of the channel in immunoprecipitates, an effect that was stimulated by AMP and inhibited by compound C. Our findings demonstrate a central role for AMPK in stimulus-response coupling by hypoxia and identify for the first time a link between metabolic stress and ion channel regulation in an O2-sensing system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.