ArticleBritish journal of pharmacology2014
Bitter tasting compounds dilate airways by inhibiting airway smooth muscle calcium oscillations and calcium sensitivity.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 85 citations in OpenAlex.
- Mechanically induced dysregulation of calcium homeostasis: a molecular linchpin in asthmatic pathogenesis.European journal of medical research · 2025Review
- Spatiotemporal calcium signaling patterns underlying opposing effects of histamine and TAS2R agonists in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Article
- High throughput screening of airway constriction in mouse lung slices.Scientific reports · 2024Article
- Molecular mechanism of bitter taste receptor agonist-mediated relaxation of airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.Respiratory research · 2024Review
- Phenanthroline relaxes uterine contractions induced by diverse contractile agents by decreasing cytosolic calcium concentration.European journal of pharmacology · 2024Article
- Perspectives on precision cut lung slices-powerful tools for investigation of mechanisms and therapeutic targets in lung diseases.Frontiers in pharmacology · 2023Review
- Review
- Article
- Bitter Taste Receptors in the Airway Cells Functions.Handbook of experimental pharmacology · 2022Article
- Chloroquine Attenuates Asthma Development by Restoring Airway Smooth Muscle Cell PhenotypeFrontiers in pharmacology · 2022Article
- The bitter end: T2R bitter receptor agonists elevate nuclear calcium and induce apoptosis in non-ciliated airway epithelial cells.Cell calcium · 2022Article
- An update on extra-oral bitter taste receptors.Journal of translational medicine · 2021Review
- Genetic deletion of the Tas2r143/Tas2r135/Tas2r126 cluster reveals that TAS2Rs may not mediate bitter tastant-induced bronchodilation.Journal of cellular physiology · 2021Article
- Oscillating calcium signals in smooth muscle cells underlie the persistent basal tone of internal anal sphincter.Journal of cellular physiology · 2021Article
- Stiffening of the extracellular matrix is a sufficient condition for airway hyperreactivity.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Possible Beneficial Actions of Caffeine in SARS-CoV-2.International journal of molecular sciences · 2021Review
- Reduced biomechanical models for precision-cut lung-slice stretching experiments.Journal of mathematical biology · 2021Article
- Can GPCRs Be Targeted to Control Inflammation in Asthma?Advances in experimental medicine and biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeWhile selective, bitter tasting, TAS2R agonists can relax agonist-contracted airway smooth muscle (ASM), their mechanism of action is unclear. However, ASM contraction is regulated by Ca²⁺ signalling and Ca²⁺ sensitivity. We have therefore investigated how the TAS2R10 agonists chloroquine, quinine and denotonium regulate contractile agonist-induced Ca²⁺ signalling and sensitivity. EXPERIMENTAL APPROACH: Airways in mouse lung slices were contracted with either methacholine (MCh) or 5HT and bronchodilation assessed using phase-contrast microscopy. Ca²⁺ signalling was measured with 2-photon fluorescence microscopy of ASM cells loaded with Oregon Green, a Ca²⁺-sensitive indicator (with or without caged-IP₃). Effects on Ca²⁺ sensitivity were assessed on lung slices treated with caffeine and ryanodine to permeabilize ASM cells to Ca²⁺ . KEY
resultsThe TAS2R10 agonists dilated airways constricted by either MCh or 5HT, accompanied by inhibition of agonist-induced Ca²⁺ oscillations. However, in non-contracted airways, TAS2R10 agonists, at concentrations that maximally dilated constricted airways, did not evoke Ca²⁺ signals in ASM cells. Ca²⁺ increases mediated by the photolysis of caged-IP₃ were also attenuated by chloroquine, quinine and denotonium. In Ca²⁺-permeabilized ASM cells, the TAS2R10 agonists dilated MCh- and 5HT-constricted airways. CONCLUSIONS AND IMPLICATIONS: TAS2R10 agonists reversed bronchoconstriction by inhibiting agonist-induced Ca²⁺ oscillations while simultaneously reducing the Ca²⁺ sensitivity of ASM cells. Reduction of Ca²⁺ oscillations may be due to inhibition of Ca²⁺ release through IP₃ receptors. Further characterization of bronchodilatory TAS2R agonists may lead to the development of novel therapies for the treatment of bronchoconstrictive conditions.
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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.