ArticleThe Journal of physiology2007
Modulation of TASK-like background potassium channels in rat arterial chemoreceptor cells by intracellular ATP and other nucleotides.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 82 citations in OpenAlex.
- Acute Hypoxia Inhibits KActa physiologica (Oxford, England) · 2026Article
- Physiological Differences Underlying Divergent Hypoxia Responses and Altitude Adaptations in Humans, Rats and Mice.Comprehensive Physiology · 2025Review
- Reactive Oxidative Species in Carotid Body Chemoreception: Their Role in Oxygen Sensing and Cardiorespiratory Alterations Induced by Chronic Intermittent Hypoxia.Antioxidants (Basel, Switzerland) · 2025Review
- Expression and function of mitochondrial inhibitor factor-1 and TASK channels in adrenal cells.Biochemical and biophysical research communications · 2023Article
- Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023Review
- Of Mice and Men and Plethysmography Systems: Does LKB1 Determine the Set Point of Carotid Body Chemosensitivity and the Hypoxic Ventilatory Response?Advances in experimental medicine and biology · 2023Article
- Insights into the control and consequences of breathing adjustments in fishes-from larvae to adults.Frontiers in physiology · 2023Review
- LKB1 is the gatekeeper of carotid body chemosensing and the hypoxic ventilatory response.Communications biology · 2022Article
- Are Multiple Mitochondrial Related Signalling Pathways Involved in Carotid Body Oxygen Sensing?Frontiers in physiology · 2022Review
- Acute Oxygen-SensingFrontiers in physiology · 2022Article
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Mitochondrial Succinate Metabolism and Reactive Oxygen Species Are Important but Not Essential for Eliciting Carotid Body and Ventilatory Responses to Hypoxia in the Rat.Antioxidants (Basel, Switzerland) · 2021Article
- Molecular Mechanisms of Acute Oxygen Sensing by Arterial Chemoreceptor Cells. Role of Hif2α.Frontiers in physiology · 2020Review
- Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms.The Journal of physiology · 2018Review
- Carotid Body Type-I Cells Under Chronic Sustained Hypoxia: Focus on Metabolism and Membrane Excitability.Frontiers in physiology · 2018Article
- Is Carotid Body Physiological OFrontiers in physiology · 2018Review
- Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals.Frontiers in physiology · 2018Review
- Redox signaling in acute oxygen sensing.Redox biology · 2017Review
- The emerging role of AMPK in the regulation of breathing and oxygen supply.The Biochemical journal · 2016Review
- Moderate inhibition of mitochondrial function augments carotid body hypoxic sensitivity.Pflugers Archiv : European journal of physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The carotid body's physiological role is to sense arterial oxygen, CO(2) and pH. It is however, also powerfully excited by inhibitors of oxidative phosphorylation. This latter observation is the cornerstone of the mitochondrial hypothesis which proposes that oxygen is sensed through changes in energy metabolism. All of these stimuli act in a similar manner, i.e. by inhibiting a background TASK-like potassium channel (K(B)) they induce membrane depolarization and thus neurosecretion. In this study we have evaluated the role of ATP in modulating K(B) channels. We find that K(B) channels are strongly activated by MgATP (but not ATP(4)(-)) within the physiological range (K(1/2) = 2.3 mm). This effect was mimicked by other Mg-nucleotides including GTP, UTP, AMP-PCP and ATP-gamma-S, but not by PP(i) or AMP, suggesting that channel activity is regulated by a Mg-nucleotide sensor. Channel activation by MgATP was not antagonized by either 1 mm AMP or 500 microm ADP. Thus MgATP is probably the principal nucleotide regulating channel activity in the intact cell. We therefore investigated the effects of metabolic inhibition upon both [Mg(2+)](i), as an index of MgATP depletion, and channel activity in cell-attached patches. The extent of increase in [Mg(2+)](i) (and thus MgATP depletion) in response to inhibition of oxidative phosphorylation were consistent with a decline in [MgATP](i) playing a prominent role in mediating inhibition of K(B) channel activity, and the response of arterial chemoreceptors to metabolic compromise.
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