ArticleEMBO reports2007
Altered acetylcholine, bradykinin and cutaneous pressure-induced vasodilation in mice lacking the TREK1 potassium channel: the endothelial link.
Article in EMBO reports, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 83 citations in OpenAlex.
- Role for TREK-1 as a polymodal sensor and regulator of cell activity.Channels (Austin, Tex.) · 2026Review
- Mechanosensing by Vascular Endothelium.Annual review of physiology · 2024Review
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Magnetic activation of TREK1 triggers stress signalling and regulates neuronal branching in SH-SY5Y cells.Frontiers in medical technology · 2022Article
- Mechanotransduction at the Plasma Membrane-Cytoskeleton Interface.International journal of molecular sciences · 2021Review
- Negative Influence by the Force: Mechanically Induced Hyperpolarization via KInternational journal of molecular sciences · 2021Review
- Aging Affects KFrontiers in physiology · 2021Article
- PIPInternational journal of molecular sciences · 2020Article
- Alteration of Pressure-Induced Vasodilation in Aging and Diabetes, a Neuro-Vascular Damage.Frontiers in physiology · 2019Article
- The two-pore domain potassium channel TREK-1 mediates cardiac fibrosis and diastolic dysfunction.The Journal of clinical investigation · 2018Article
- Asymmetric mechanosensitivity in a eukaryotic ion channel.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- An allosteric ligand-binding site in the extracellular cap of K2P channels.Nature communications · 2017Article
- Two-Pore K+ Channel TREK-1 Regulates Sinoatrial Node Membrane Excitability.Journal of the American Heart Association · 2016Article
- In-Depth Study of the Interaction, Sensitivity, and Gating Modulation by PUFAs on KFrontiers in physiology · 2016Review
- The family of K2P channels: salient structural and functional properties.The Journal of physiology · 2015Review
- Much more than a leak: structure and function of K₂p-channels.Pflugers Archiv : European journal of physiology · 2015Review
- Trek1 contributes to maintaining nasal epithelial barrier integrity.Scientific reports · 2015Article
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
- Molecular aspects of structure, gating, and physiology of pH-sensitive background K2P and Kir K+-transport channels.Physiological reviews · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The TWIK related K+ channel TREK1 is an important member of the class of two-pore-domain K+ channels. It is a background K+ channel and is regulated by hormones, neurotransmitters, intracellular pH and mechanical stretch. This work shows that TREK1 is present both in mesenteric resistance arteries and in skin microvessels. It is particularly well expressed in endothelial cells. Deletion of TREK1 in mice leads to an important alteration in vasodilation of mesenteric arteries induced by acetylcholine and bradykinin. Iontophoretic delivery of acetylcholine and bradykinin in the skin of TREK1+/+ and TREK1-/- mice also shows the important role of TREK1 in cutaneous endothelium-dependent vasodilation. The vasodilator response to local pressure application is also markedly decreased in TREK1-/- mice, mimicking the decreased response to pressure observed in diabetes. Deletion of TREK1 is associated with a marked alteration in the efficacy of the G-protein-coupled receptor-associated cascade producing NO that leads to major endothelial dysfunction.
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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.