ArticleThe Journal of physiology2002
Hypoxia inhibits human recombinant large conductance, Ca(2+)-activated K(+) (maxi-K) channels by a mechanism which is membrane delimited and Ca(2+) sensitive.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 76 citations in OpenAlex.
- Antioxidants prevent depression of the acute hypoxic ventilatory response by subanaesthetic halothane in men.The Journal of physiology · 2002Trial
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Intracellular activation of full-length human TREK-1 channel by hypoxia, high lactate, and low pH denotes polymodal integration by ischemic factors.Pflugers Archiv : European journal of physiology · 2021Article
- Hypoxic Regulation of the Large-Conductance, Calcium and Voltage-Activated Potassium Channel, BK.Frontiers in physiology · 2021Review
- FeACS chemical biology · 2020Article
- Functional Interactions between BKOxidative medicine and cellular longevity · 2016Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- A review on hemeoxygenase-2: focus on cellular protection and oxygen response.Oxidative medicine and cellular longevity · 2014Review
- Calcium-activated potassium channels in ischemia reperfusion: a brief update.Frontiers in physiology · 2014Review
- K(+) channels in O(2) sensing and postnatal development of carotid body glomus cell response to hypoxia.Respiratory physiology & neurobiology · 2013Review
- Function and regulation of large conductance Ca(2+)-activated K+ channel in vascular smooth muscle cells.Drug discovery today · 2012Review
- Peripheral chemoreceptors: function and plasticity of the carotid body.Comprehensive Physiology · 2012Review
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Alveolar epithelial CNGA1 channels mediate cGMP-stimulated, amiloride-insensitive, lung liquid absorption.Pflugers Archiv : European journal of physiology · 2011Article
- Endothelial and smooth muscle cell ion channels in pulmonary vasoconstriction and vascular remodeling.Comprehensive Physiology · 2011Review
- Identification of a thiol/disulfide redox switch in the human BK channel that controls its affinity for heme and CO.The Journal of biological chemistry · 2010Article
- Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?Progress in neurobiology · 2010Review
- Alpha5beta1 integrin engagement increases large conductance, Ca2+-activated K+ channel current and Ca2+ sensitivity through c-src-mediated channel phosphorylation.The Journal of biological chemistry · 2010Article
- Heteromeric TASK-1/TASK-3 is the major oxygen-sensitive background K+ channel in rat carotid body glomus cells.The Journal of physiology · 2009Article
- Distribution of voltage-gated potassium and hyperpolarization-activated channels in sensory afferent fibers in the rat carotid body.The Journal of comparative neurology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Large conductance, Ca(2+)-activated K(+) (maxi-K ) channel activity was recorded in excised, inside-out patches from HEK 293 cells stably co-expressing the alpha- and beta-subunits of human brain maxi-K channels. At +50 mV, and in the presence of 300 nM Ca2+i, single channel activity was acutely and reversibly suppressed upon reducing P(O(2)) from 150 to > 40 mmHg by over 30 %. The hypoxia-evoked reduction in current was due predominantly to suppression in NP(o), although a minor component was attributable to reduced unitary conductance of 8-12 %. Hypoxia caused an approximate doubling of the time constant for activation but was without effect on deactivation. At lower levels of Ca2+i(30 and 100 nM), hypoxic inhibition did not reach significance. In contrast, 300 nM and 1 microM Ca2+i both sustained significant hypoxic suppression of activity over the entire activating voltage range. At these two Ca2+i levels, hypoxia evoked a positive shift in the activating voltage (by approximately 10 mV at 300 nM and approximately 25 mV at 1 microM). At saturating [Ca(2+)](i) (100 microM), hypoxic inhibition was absent. Distinguishing between hypoxia-evoked changes in voltage- and/or Ca2+i-sensitivity was achieved by evoking maximal channel activity using high depolarising potentials (up to +200 mV) in the presence of 300 nM or 100 microM Ca2+i or in its virtual absence (> 1 nM). Under these experimental conditions, hypoxia caused significant channel inhibition only in the presence of 300 nM Ca2+i. Thus, since regulation was observed in excised patches, maxi-K channel inhibition by hypoxia does not require soluble intracellular components and, mechanistically, is voltage independent and Ca2+i sensitive.
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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.