ArticleScientific reports2025
Amitriptyline inhibits bronchoconstriction independent of direct receptor binding and reduces number of caveolae.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Effects of Inhaled Amitriptyline on Airway Function and Immune Responses in Experimental Asthma.Advances in respiratory medicine · 2026Article
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Bronchial asthma is a chronic inflammatory disease with rising prevalence worldwide. Apart from the immunological role of the tricyclic antidepressant amitriptyline in bronchial asthma, there is emerging evidence that inhaled amitriptyline directly reduces acute bronchoconstriction. However, the mechanism by which amitriptyline influences bronchial tone remains poorly understood. To influence bronchoconstriction, rat precision-cut lung slices treated with varying concentrations of amitriptyline (0-5 µM) and incubated with inhibitors targeting different signaling pathways. Amitriptyline reduces acetylcholine- and serotonin-induced bronchoconstriction. Neither the muscarinic antagonist ipratropium nor the phospholipase C inhibitor U73122, nor the protein kinase C inhibitor chelerythrine diminished the effect of amitriptyline. Inhibition of calcium sensitizing and induction failed to alter amitriptyline's effect on bronchoconstriction. Caveolae-as part of the plasma membrane-display a microenvironment, where regulation of signal transduction takes place. Similar to methyl ß cyclodextrin (MBCD), a common substance to destroy caveolae, amitriptyline dramatically reduced the number of caveolae in lung tissue. However, unlike MBCD, this effect could not be explained by cholesterol depletion alone, as cholesterol repletion did not reverse amitriptyline's effect. Furthermore, neither simvastatin (a lipid lowering agent) nor cytochalasin D (an inhibitor of actin polymerization), influenced the inhibitory effect of amitriptyline on bronchoconstriction. In conclusion, amitriptyline inhibits bronchoconstriction independently of direct receptor binding or interaction. It also reduces the total number of caveolae without effects on cholesterol lowering pathways or actin depolymerization. A more general mechanism seems likely, as inhibition of single signal transduction pathways failed. Further studies are required to elucidate the underlying mechanisms.
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Registered trials
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