ArticleThe Journal of physiology2008
Block of inhibitory junction potentials and TREK-1 channels in murine colon by Ca2+ store-active drugs.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- 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
- Bepridil, a class IV antiarrhythmic agent, can block the TREK-1 potassium channel.Annals of translational medicine · 2021Article
- Protein kinase A facilitates relaxation of mouse ileum via phosphorylation of neuronal nitric oxide synthase.British journal of pharmacology · 2020Article
- Altered detrusor contractility and voiding patterns in mice lacking the mechanosensitive TREK-1 channel.BMC urology · 2019Article
- Branched Short-Chain Fatty Acid Isovaleric Acid Causes Colonic Smooth Muscle Relaxation via cAMP/PKA Pathway.Digestive diseases and sciences · 2019Article
- Nitric oxide and its role as a non-adrenergic, non-cholinergic inhibitory neurotransmitter in the gastrointestinal tract.British journal of pharmacology · 2019Review
- Involvement of intracellular transport in TREK-1c current run-up in 293T cells.Channels (Austin, Tex.) · 2017Article
- Mechanosensitive Piezo Channels in the Gastrointestinal Tract.Current topics in membranes · 2017Review
- Gastrointestinal motility and its enteric actors in mechanosensitivity: past and present.Pflugers Archiv : European journal of physiology · 2015Review
- Protein kinase A and C regulate leak potassium currents in freshly isolated vascular myocytes from the aorta.PloS one · 2013Article
- Ionic conductances regulating the excitability of colonic smooth muscles.Neurogastroenterology and motility · 2012Review
- Expression level of Hand2 affects specification of enteric neurons and gastrointestinal function in mice.Gastroenterology · 2011Article
- Expression of stretch-activated two-pore potassium channels in human myometrium in pregnancy and labor.PloS one · 2010Article
- TREK-1 channels do not mediate nitrergic neurotransmission in circular smooth muscle from the lower oesophageal sphincter.British journal of pharmacology · 2010Article
- Concepts of neural nitric oxide-mediated transmission.The European journal of neuroscience · 2008Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Post-junctional enteric inhibitory responses are composed of at least two components attributed to the release of a purine and nitric oxide (NO). The nitrergic component is characterized by membrane potential hyperpolarization; however, the conductances involved and the role of Ca(2+) stores in regulating these conductances are controversial. Conventional microelectrode recordings were performed in intact muscle strips and whole-cell voltage clamp experiments were performed on freshly dispersed cells and COS7 cells stably transfected with TREK-1 channels. Here we show that several Ca(2+) store-active compounds, including caffeine, ryanodine, and cyclopiazonic acid, reduce inhibitory junction potentials and responses to sodium nitroprusside in murine colonic muscles. We previously proposed that two-pore K(+) channels of the TREK family mediate a portion of the hyperpolarization response to NO in colonic muscles. We tested the effects of Ca(2+) store-active drugs in COS cells expressing murine TREK-1 channels and found these compounds block TREK-1 currents. These effects were greatly attenuated by dialysing cells with protein kinase A inhibitory peptide (PKAI). Caffeine also blocked stretch-dependent K(+) (SDK) channels, thought to be due to expression of TREK channels, in colonic myocytes, but these effects were not apparent in excised patches. Taken together our data show that Ca(2+) store-active compounds inhibit TREK-1 channels, native SDK channels, and nitrergic inhibitory junction potentials. These effects appear to be due, in part, to the cAMP/PKA stimulatory actions of these drugs and inhibitory effects of TREK channels.
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What OpenQuestion holds
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.