ArticleNeurourology and urodynamics2009
Bladder urothelial cells from patients with interstitial cystitis have an increased sensitivity to carbachol.
Article in Neurourology and urodynamics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Pain in Inflammatory Bowel Disease: Optogenetic Strategies for Study of Neural-Epithelial Signaling.Crohn's & colitis 360 · 2021Review
- Expression of components of the urothelial cholinergic system in bladder and cultivated primary urothelial cells of the pig.BMC urology · 2019Article
- Urinary bladder, cystitis and nerve/urothelial interactions.Autonomic neuroscience : basic & clinical · 2014Review
- Evidence for bladder urothelial pathophysiology in functional bladder disorders.BioMed research international · 2014Review
- Urothelial signaling.Physiological reviews · 2013Review
- Alterations in the non-neuronal acetylcholine synthesis and release machinery in esophageal epithelium.Life sciences · 2012Article
- Cell biology and physiology of the uroepithelium.American journal of physiology. Renal physiology · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsThe presence of muscarinic receptors on bladder urothelial cells (BUC), suggests BUC may be a target for antimuscarinics. This study determined whether human BUC are responsive to a muscarinic agonist and if so, whether responses are altered in interstitial cystitis (IC) BUC.
methodsPrimary urothelial cell cultures were established from cystoscopic biopsies. Normal (NB) and IC BUC were studied using calcium imaging techniques as a means to monitor the response to muscarinic receptor activation with the agonist, carbachol (CCh). Changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) were measured with fura-2 ratiometric microfluorimetry. Dose-response curves (CCh dose vs. [Ca(2+)](i)) were measured in IC and NB BUC. Tolterodine was used to confirm the specificity (muscarinic versus nicotinic) of CCh evoked increases in [Ca(2+)](i).
resultsCCh induced a dose-dependent increase in [Ca(2+)](i). Potency and efficacy of CCh was significantly greater in IC BUC. The maximal increase in [Ca(2+)](i) was 136.3 +/- 5.1% over baseline in 78 cells from 4 IC patients versus 92.4 +/- 4.8% over baseline in 67 cells from 4 NB subjects (P < 0.01). The EC50 of the evoked increase was 1.10 +/- 0.14 microM versus 3.36 +/- 0.72 microM (P < 0.01) in BUC from IC and NB controls, respectively. Removal of extracellular calcium or application of tolterodine, abolished CCh evoked increase in [Ca(2+)](i) in IC and NB BUC.
conclusionsThe greater sensitivity of IC BUC to CCh suggests that IC patholobiology may also include alterations muscarinic signaling. The physiologic sequelae of muscarinic activation in BUC need to be further investigated.
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