ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
HCl-activated neural and epithelial vanilloid receptors (TRPV1) in cat esophageal mucosa.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. 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.
- Radiofrequency ablation reduces esophageal hypersensitivity in refractory non-erosive reflux disease.Frontiers in medicine · 2026Article
- Sensory Phenotype of the Oesophageal Mucosa in Gastro-Oesophageal Reflux Disease.International journal of molecular sciences · 2023Review
- Changes in Elements and Relationships among Elements in Intervertebral Disc Degeneration.International journal of environmental research and public health · 2022Article
- Efficacy of Endoscopic Radiofrequency Ablation for Treatment of Reflux Hypersensitivity: A Study Based on Rome IV Criteria.Gastroenterology research and practice · 2022Article
- Exploration of the Esophageal Mucosal Barrier in Non-Erosive Reflux Disease.International journal of molecular sciences · 2017Article
- Capsaicin, Nociception and Pain.Molecules (Basel, Switzerland) · 2016Review
- Upregulation of Vanilloid Receptor-1 in Functional Dyspepsia With or Without Helicobacter pylori Infection.Medicine · 2016Article
- Human esophageal myofibroblasts secrete proinflammatory cytokines in response to acid and Toll-like receptor 4 ligands.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Distribution of transient receptor potential cation channel subfamily V member 1-expressing nerve fibers in mouse esophagus.Histochemistry and cell biology · 2014Article
- Transient receptor potential cation channels in visceral sensory pathways.British journal of pharmacology · 2014Review
- Platelet-activating factor and distinct chemokines are elevated in mucosal biopsies of erosive compared with non-erosive reflux disease patients and controls.Neurogastroenterology and motility · 2012Article
- HCl-induced and ATP-dependent upregulation of TRPV1 receptor expression and cytokine production by human esophageal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- ATP: a mediator for HCl-induced TRPV1 activation in esophageal mucosa.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- Gastroesophageal reflux disease--from reflux episodes to mucosal inflammation.Nature reviews. Gastroenterology & hepatology · 2011Review
- Transient receptor potential (TRP) channels as drug targets for diseases of the digestive system.Pharmacology & therapeutics · 2011Review
- Cystitis, co-morbid disorders and associated epithelial dysfunction.Neurourology and urodynamics · 2011Review
- TRP channels in neurogastroenterology: opportunities for therapeutic intervention.British journal of pharmacology · 2011Review
- TRP channels in the digestive system.Current pharmaceutical biotechnology · 2011Review
- Viewpoints on Acid-induced inflammatory mediators in esophageal mucosa.Journal of neurogastroenterology and motility · 2010Article
- HCl-induced inflammatory mediators in esophageal mucosa increase migration and production of H2O2 by peripheral blood leukocytes.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
To test whether transient receptor potential channel vanilloid subfamily member-1 (TRPV1) mediates acid-induced inflammation in the esophagus, a tubular segment of esophageal mucosa was tied at both ends, forming a sac. The sac was filled with 0.01 N HCl (or Krebs buffer for control) and kept in oxygenated Krebs buffer at 37 degrees C. The medium around the sac (supernatant) was collected after 3 h. Supernatant of the HCl-filled sac abolished contraction of esophageal circular muscle strips in response to electric field stimulation. Contraction was similarly abolished by supernatant of mucosal sac filled with the TRPV1 agonist capsaicin (10(-6) M). These effects were reversed by the selective TRPV1 antagonist 5'-iodoresiniferatoxin (IRTX) and by the platelet-activating factor (PAF) receptor antagonist CV9388. Substance P and CGRP levels in mucosa and in supernatant increased in response to HCl, and these increases were abolished by IRTX and by tetrodotoxin (TTX) but not affected by CV9388, indicating that substance P and CGRP are neurally released and PAF independent. In contrast, the increase in PAF was blocked by IRTX but not by TTX. Presence of TRPV1 receptor was confirmed by RT-PCR and by Western blot analysis in whole mucosa and in esophageal epithelial cells enzymatically isolated and sorted by flow cytometry or immunoprecipitated with cytokeratin antibodies. In epithelial cells PAF increased in response to HCl, and the increase was abolished by IRTX. We conclude that HCl-induced activation of TRPV1 receptors in esophageal mucosa causes release of substance P and CGRP from neurons and release of PAF from epithelial cells.
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