ArticleThe Journal of physiology2003
Acute hypoxia occludes hTREK-1 modulation: re-evaluation of the potential role of tandem P domain K+ channels in central neuroprotection.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- Multiple pregnancies, the myometrium and the role of mechanical factors in the timing of labour.Current research in physiology · 2023Article
- Bepridil, a class IV antiarrhythmic agent, can block the TREK-1 potassium channel.Annals of translational medicine · 2021Article
- 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
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- Myometrial relaxation of mice via expression of two pore domain acid sensitive K(+) (TASK-2) channels.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing.Pflugers Archiv : European journal of physiology · 2015Review
- Mechanism of Relaxation Via TASK-2 Channels in Uterine Circular Muscle of Mouse.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
- Pharmacological investigation of memory restorative effect of riluzole in mice.Indian journal of pharmacology · 2012Article
- Regulation and function of the two-pore-domain (K2P) potassium channel Trek-1 in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Novel neuroprotectant chiral 3-n-butylphthalide inhibits tandem-pore-domain potassium channel TREK-1.Acta pharmacologica Sinica · 2011Article
- Avian magnetite-based magnetoreception: a physiologist's perspective.Journal of the Royal Society, Interface · 2010Article
- The Inhibition of TREK2 Channel by an Oxidizing Agent, 5,5'-dithio-bis (2-nitrobenzoic acid), via Interaction with the C-terminus Distal to the 353rd Amino Acid.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008Article
- Effects of chlorpromazine and trinitrophenol on the membrane motor of outer hair cells.Biophysical journal · 2007Article
- The lipid-activated two-pore domain K+ channel TREK-1 is resistant to hypoxia: implication for ischaemic neuroprotection.The Journal of physiology · 2005Article
- The effects of hypoxia on the modulation of human TREK-1 potassium channels.The Journal of physiology · 2005Article
- The 2P-domain K+ channels: role in apoptosis and tumorigenesis.Pflugers Archiv : European journal of physiology · 2004Review
- Regulation of recombinant human brain tandem P domain K+ channels by hypoxia: a role for O2 in the control of neuronal excitability?Journal of cellular and molecular medicineReview
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Authors and funding
6 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The human tandem P domain K+ channel hTREK-1 (KCNK2) is distributed widely through the CNS. Here, whole-cell patch clamp recordings were employed to investigate the effects of hypoxia on hTREK-1 channels stably expressed in human embryonic kidney cells. Acute hypoxia caused a rapid and reversible inhibition of whole-cell K+ current amplitudes; this was PO2 dependent with a maximal inhibition achieved at 60 mmHg and below. In accordance with previous studies, hTREK-1 current amplitudes were enhanced by arachidonic acid. This effect was concentration dependent, with maximal enhancement observed at a concentration of 10 microM. Membrane deformation by the crenator trinitrophenol (to mimic cell swelling) or the cup former chlorpromazine (to mimic cell shrinkage) caused robust activation and inhibition of currents, respectively. However, current augmentation by either arachidonic acid or trinitrophenol was completely prevented during hypoxia; conversely, hypoxia blunted the inhibitory action of chlorpromazine. The abilities of arachidonic acid to augment currents and of hypoxia to completely abrogate this effect were also observed in cell-attached patches. Our data indicate that hypoxia interacts with hTREK-1, and occludes its modulation by arachidonic acid and membrane deformation. These findings also suggest that the potential neuroprotective role of TREK channels, which has recently been proposed, requires reconsideration since hTREK-1 activation is unlikely when ambient PO2 is below 60 mmHg - a situation which normally pertains in the CNS even during systemic normoxia.
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