ArticleBritish journal of pharmacology2003
Activation of vanilloid receptor 1 by resiniferatoxin mobilizes calcium from inositol 1,4,5-trisphosphate-sensitive stores.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 68 citations in OpenAlex.
- Psychological stress-induced ALKBH5 deficiency promotes tumour innervation and pancreatic cancer via extracellular vesicle transfer of RNA.Nature cell biology · 2025Article
- TRPV1 Modulator Ameliorates Alzheimer-Like Amyloid-Oxidative medicine and cellular longevity · 2022Article
- Article
- TRP Channels as Emerging Therapeutic Targets for Neurodegenerative Diseases.Frontiers in physiology · 2020Review
- Capsaicin: Physicochemical properties, cutaneous reactions and potential applications in painful and inflammatory conditions.Experimental and therapeutic medicine · 2019Review
- Oxytocin Relieves Neuropathic Pain Through GABA Release and Presynaptic TRPV1 Inhibition in Spinal Cord.Frontiers in molecular neuroscience · 2018Article
- Molecular Surgery Concept from Bench to Bedside: A Focus on TRPV1+ Pain-Sensing Neurons.Frontiers in physiology · 2017Review
- Article
- Divalent heavy metal cations block the TRPV1 Ca(2+) channel.Biological trace element research · 2013Article
- The efficacy of resiniferatoxin in prevention of catheter related bladder discomfort in patients after TURP - a pilot, randomized, open study.Translational andrology and urology · 2012Article
- TRPV1: a stress response protein in the central nervous system.American journal of neurodegenerative disease · 2012Article
- TRPV1: contribution to retinal ganglion cell apoptosis and increased intracellular Ca2+ with exposure to hydrostatic pressure.Investigative ophthalmology & visual science · 2009Article
- Vanilloid-induced conduction analgesia: selective, dose-dependent, long-lasting, with a low level of potential neurotoxicity.Anesthesia and analgesia · 2008Review
- Contribution of TRPV1 to microglia-derived IL-6 and NFkappaB translocation with elevated hydrostatic pressure.Investigative ophthalmology & visual science · 2008Article
- The activation of transient receptor potential vanilloid receptor subtype 1 by capsaicin without extracellular Ca2+ is involved in the mechanism of distinct substance P release in cultured rat dorsal root ganglion neurons.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- Article
- Roles of transient receptor potential vanilloid subtype 1 and cannabinoid type 1 receptors in the brain: neuroprotection versus neurotoxicity.Molecular neurobiology · 2007Review
- Activation of transient receptor potential vanilloid 1 (TRPV1) by resiniferatoxin.The Journal of physiology · 2005Article
- Effects of piperine, the pungent component of black pepper, at the human vanilloid receptor (TRPV1).British journal of pharmacology · 2005Article
- Transient receptor potential vanilloid subtype 1 mediates cell death of mesencephalic dopaminergic neurons in vivo and in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 Capsaicin and resiniferatoxin (RTX) stimulate Ca2+ influx by activating vanilloid receptor 1 (VR1), a ligand-gated Ca2+ channel on sensory neurones. We investigated whether VR1 activation could also trigger Ca2+ mobilization from intracellular Ca2+ stores. 2 Human VR1-transfected HEK293 cells (hVR1-HEK293) were loaded with Fluo-3 or a mixture of Fluo-4 and Fura Red and imaged on a fluorometric imaging plate reader (FLIPR) and confocal microscope respectively. 3 In Ca2+ -free media, RTX caused a transient elevation in intracellular free Ca2+ concentration in hVR1-HEK293 cells (pEC(50) 6.45+/-0.05) but not in wild type cells. Capsaicin (100 microM) did not cause Ca2+ mobilization under these conditions. 4 RTX-mediated Ca2+ mobilization was inhibited by the VR1 receptor antagonist capsazepine (pIC(50) 5.84+/-0.04), the Ca2+ pump inhibitor thapsigargin (pIC(50) 7.77+/-0.04), the phospholipase C inhibitor U-73122 (pIC(50) 5.35+/-0.05) and by depletion of inositol 1,4,5-trisphosphate-sensitive Ca2+ stores by pretreatment with the acetylcholine-receptor agonist carbachol (20 microM, 2 min). These data suggest that RTX causes Ca2+ mobilization from inositol 1,4,5-trisphosphate-sensitive Ca2+ stores in hVR1-HEK293 cells. 5 In the presence of extracellular Ca2+, both capsaicin-mediated and RTX-mediated Ca2+ rises were attenuated by U-73122 (10 microM, 30 min) and thapsigargin (1 microM, 30 min). We conclude that VR1 is able to couple to Ca2+ mobilization by a Ca2+ dependent mechanism, mediated by capsaicin and RTX, and a Ca2+ independent mechanism mediated by RTX alone.
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