ArticleBritish journal of pharmacology2014
Regulation of ACh release from guinea pig bladder urothelial cells: potential role in bladder filling sensations.
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 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- Can the Bladder Itself "Measure" Volume, and Thereby Help to Determine When Initiation of Voiding Should Occur? ICI-RS 2024.Neurourology and urodynamics · 2025Review
- Uropathogenic Escherichia coli causes significant urothelial damage in an ex vivo porcine bladder model, with no protective effect observed from cranberry or d-mannose.Pathogens and disease · 2024Article
- Review
- Purinergic signalling in the urinary bladder - When function becomes dysfunction.Autonomic neuroscience : basic & clinical · 2021Article
- Cystic fibrosis transmembrane conductance regulator modulates enteric cholinergic activities and is abnormally expressed in the enteric ganglia of patients with slow transit constipation.Journal of gastroenterology · 2019Article
- The Botulinum Treatment of Neurogenic Detrusor Overactivity: The Double-Face of the Neurotoxin.Toxins · 2019Review
- Feline Interstitial Cystitis Enhances Mucosa-Dependent Contractile Responses to Serotonin.International neurourology journal · 2018Article
- NKA enhances bladder-afferent mechanosensitivity via urothelial and detrusor activation.American journal of physiology. Renal physiology · 2018Article
- Modulation of lower urinary tract smooth muscle contraction and relaxation by the urothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2018Review
- The Emerging Role of Inflammasomes as Central Mediators in Inflammatory Bladder Pathology.Current urology · 2018Review
- TRPV1 enhances the afferent response to P2X receptor activation in the mouse urinary bladder.Scientific reports · 2018Article
- Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.The Journal of physiology · 2016Article
- The Role of the Mucosa in Normal and Abnormal Bladder Function.Basic & clinical pharmacology & toxicology · 2016Review
- Enhanced urothelial ATP release and contraction following intravesical treatment with the cytotoxic drug, doxorubicin.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Signalling molecules in the urothelium.BioMed research international · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe aim of this study was to quantify and characterize the mechanism of non-neuronal ACh release from bladder urothelial cells and to determine if urothelial cells could be a site of action of anti-muscarinic drugs. EXPERIMENTAL APPROACH: A novel technique was developed whereby ACh could be measured from freshly isolated guinea pig urothelial cells in suspension following mechanical stimulation. Various agents were used to manipulate possible ACh release pathways in turn and to study the effects of muscarinic receptor activation and inhibition on urothelial ATP release. KEY
resultsMinimal mechanical stimulus achieved full ACh release, indicating a small dynamic range and possible all-or-none signal. ACh release involved a mechanism dependent on the anion channel CFTR and intracellular calcium concentration, but was independent of extracellular calcium, vesicular trafficking, connexins or pannexins, organic cation transporters and was not affected by botulinum-A toxin. Stimulating ACh receptors increased ATP production and antagonizing them reduced ATP release, suggesting a link between ACh and ATP release. CONCLUSIONS AND IMPLICATIONS: These results suggest that release of non-neuronal ACh from the urothelium is large enough and well located to act as a modulator of ATP release. It is hypothesized that this pathway may contribute to the actions of anti-muscarinic drugs in reducing the symptoms of lower urinary tract syndromes. Additionally the involvement of CFTR in ACh release suggests an exciting new direction for the treatment of these 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.