ArticleThe journal of pain2014
ATP release mechanisms of endothelial cell-mediated stimulus-dependent hyperalgesia.
Article in The journal of pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Contractions of ex-vivo mouse bladder driven by activation of channelrhodopsin-2 expressed in urothelial cells.Scientific reports · 2025Article
- Role of ATP in migraine mechanisms: focus on P2X3 receptors.The journal of headache and pain · 2023Review
- Relationship of PIEZO1 and PIEZO2 vascular expression with diabetic neuropathy.Frontiers in physiology · 2023Article
- Association of neovascular age-related macular degeneration with migraine.Scientific reports · 2022Article
- Infrapatellar Fat Pad-Synovial Membrane Anatomo-Fuctional Unit: Microscopic Basis for Piezo1/2 Mechanosensors Involvement in Osteoarthritis Pain.Frontiers in cell and developmental biology · 2022Article
- Article
- Neurovascular contributions to migraine: Moving beyond vasodilation.Neuroscience · 2016Review
- Contribution of Piezo2 to endothelium-dependent pain.Molecular pain · 2015Article
- Regulation of alternative VEGF-A mRNA splicing is a therapeutic target for analgesia.Neurobiology of disease · 2014Article
- Cortical spreading depression and meningeal nociception.Neurobiology of pain (Cambridge, Mass.)Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledEndothelin-1 (ET-1) acts on endothelial cells to enhance mechanical stimulation-induced release of adenosine triphosphate (ATP), which in turn can act on sensory neurons innervating blood vessels to contribute to vascular pain, a phenomenon we have referred to as stimulus-dependent hyperalgesia (SDH). In the present study, we evaluated the role of the major classes of ATP release mechanisms to SDH: vesicular exocytosis, plasma membrane-associated ATP synthase, ATP-binding cassette transporters, and ion channels. Inhibitors of vesicular exocytosis (ie, monensin, brefeldin A, and bafilomycin), plasma membrane-associated ATPase (ie, oligomycin and pigment epithelium-derived factor peptide 34-mer), and connexin ion channels (carbenoxolone and flufenamic acid) but not ATP-binding cassette transporter (ie, dipyridamole, nicardipine, or CFTRinh-172) attenuated SDH. This study reports a role of ATP in SDH and suggests novel targets for the treatment of vascular pain syndromes. PERSPECTIVE: ET-1 acts on endothelial cells to produce mechanical stimulation-induced hyperalgesia. Inhibitors of 3 different ATP release mechanisms attenuated this SDH. This study provides support for a role of ATP in SDH and suggests novel targets for the treatment of vascular pain syndromes.
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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 Socratic graph.