ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2010
Cerebrovascular responses in mice deficient in the potassium channel, TREK-1.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- TREK-1 and TREK-2 Knockout Mice Are Not Resistant to Halothane or Isoflurane.Anesthesiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- The Two-Pore Domain Potassium Channel TREK-1 Promotes Blood-Brain Barrier Breakdown and Exacerbates Neuronal Death After Focal Cerebral Ischemia in Mice.Molecular neurobiology · 2022Article
- Omega-3 Polyunsaturated Fatty Acids-Vascular and Cardiac Effects on the Cellular and Molecular Level (Narrative Review).International journal of molecular sciences · 2022Review
- Negative Influence by the Force: Mechanically Induced Hyperpolarization via KInternational journal of molecular sciences · 2021Review
- TREK-1 Null Impairs Neuronal Excitability, Synaptic Plasticity, and Cognitive Function.Molecular neurobiology · 2020Article
- TREK-1 protects the heart against ischemia-reperfusion-induced injury and from adverse remodeling after myocardial infarction.Pflugers Archiv : European journal of physiology · 2019Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- Altered detrusor contractility and voiding patterns in mice lacking the mechanosensitive TREK-1 channel.BMC urology · 2019Article
- Deficiency of TREK-1 potassium channel exacerbates blood-brain barrier damage and neuroinflammation after intracerebral hemorrhage in mice.Journal of neuroinflammation · 2019Article
- The two-pore domain potassium channel TREK-1 mediates cardiac fibrosis and diastolic dysfunction.The Journal of clinical investigation · 2018Article
- Genetic Deletion of TREK-1 or TWIK-1/TREK-1 Potassium Channels does not Alter the Basic Electrophysiological Properties of Mature Hippocampal Astrocytes In Situ.Frontiers in cellular neuroscience · 2016Article
- Activation of endothelial transient receptor potential C3 channel is required for small conductance calcium-activated potassium channel activation and sustained endothelial hyperpolarization and vasodilation of cerebral artery.Journal of the American Heart Association · 2014Article
- Temperature sensitivity of two-pore (K2P) potassium channels.Current topics in membranes · 2014Review
- Alterations of N-3 polyunsaturated fatty acid-activated K2P channels in hypoxia-induced pulmonary hypertension.Basic & clinical pharmacology & toxicology · 2013Article
- Endothelial TWIK-related potassium channel-1 (TREK1) regulates immune-cell trafficking into the CNS.Nature medicine · 2013Article
- A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells.Journal of neurophysiology · 2013Article
- Protein kinase A and C regulate leak potassium currents in freshly isolated vascular myocytes from the aorta.PloS one · 2013Article
- Traumatic brain injury in mice lacking the K channel, TREK-1.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
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8 authors at 3 institutions in 4 countries.
Funding
Abstract
We tested the hypothesis that TREK-1, a two-pore domain K channel, is involved with dilations in arteries. Because there are no selective activators or inhibitors of TREK-1, we generated a mouse line deficient in TREK-1. Endothelium-mediated dilations were not different in arteries from wild-type (WT) and TREK-1 knockout (KO) mice. This includes dilations of the middle cerebral artery to ATP, dilations of the basilar artery to ACh, and relaxations of the aorta to carbachol, a cholinergic agonist. The nitric oxide (NO) and endothelium-dependent hyperpolarizing factor components of ATP dilations were identical in the middle cerebral arteries of WT and TREK-1 KO mice. Furthermore, the NO and cyclooxygenase-dependent components were identical in the basilar arteries of the different genotypes. Dilations of the basilar artery to alpha-linolenic acid, an activator of TREK-1, were not affected by the absence of TREK-1. Whole cell currents recorded using patch-clamp techniques were similar in cerebrovascular smooth muscle cells (CVSMCs) from WT and TREK-1 KO mice. alpha-linolenic acid or arachidonic acid increased whole cell currents in CVSMCs from both WT and TREK-1 KO mice. The selective blockers of large-conductance Ca-activated K channels, penitrem A and iberiotoxin, blocked the increased currents elicited by either alpha-linolenic or arachidonic acid. In summary, dilations were similar in arteries from WT and TREK-1 KO mice. There was no sign of TREK-1-like currents in CVSMCs from WT mice, and there were no major differences in currents between the genotypes. We conclude that regulation of arterial diameter is not altered in mice lacking TREK-1.
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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.