ArticleAmerican journal of physiology. Renal physiology2017
OAB without an overactive bladder in the acute prostaglandin E2 rat model.
Article in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Cells and ionic conductances contributing to spontaneous activity in bladder and urethral smooth muscle.The Journal of physiology · 2026Review
- Effect of Bladder Injections of Botulinum Neurotoxin A on Biomarkers Associated with Inflammation and Urinary Infections in Patients with Neurogenic Detrusor Overactivity-Associated Incontinence: A Pilot, Prospective, Human Study.International journal of molecular sciences · 2026Article
- PGE2 binding to EP2 promotes ureteral stone expulsion by relaxing ureter via the cAMP-PKA pathway.BMC urology · 2024Article
- Pathways and parameters of sacral neuromodulation in rats.American journal of physiology. Renal physiology · 2023Article
- The mast cell stimulator compound 48/80 causes urothelium-dependent increases in murine urinary bladder contractility.American journal of physiology. Renal physiology · 2023Article
- The effect of botulinum toxin on ureteral inflammation.World journal of urology · 2021Article
- PGE2 receptors in detrusor muscle: Drugging the undruggable for urgency.Biochemical pharmacology · 2021Review
- Effects of intravesical prostaglandin EAmerican journal of physiology. Renal physiology · 2021Article
- State-dependent bioelectronic interface to control bladder function.Scientific reports · 2021Article
- Stimulation of the pelvic nerve increases bladder capacity in the PGEAmerican journal of physiology. Renal physiology · 2020Article
- Real-Time Bladder Pressure Estimation for Closed-Loop Control in a Detrusor Overactivity Model.IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society · 2019Article
- Detection of Bladder Contractions From the Activity of the External Urethral Sphincter in Rats Using Sparse Regression.IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society · 2018Article
- CaThe Journal of physiology · 2018Article
- Stimulation of the sensory pudendal nerve increases bladder capacity in the rat.American journal of physiology. Renal physiology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Intravesical prostaglandin E2 (PGE2) was previously used to induce overactive bladder (OAB) symptoms, as it reduces bladder capacity in rats and causes a "strong urgency sensation" in healthy women. However, the mechanism by which this occurs is unclear. To clarify how PGE2 reduces bladder capacity, 100 µM PGE2 was administered intravesically during open, single-fill cystometry with simultaneous measurement of sphincter EMG in the urethane-anesthetized female Wistar rat. PGE2 was also applied to the urethra or bladder selectively by use of a ligature at the bladder neck before (urethra) or during (bladder) closed-outlet, single-fill cystometry. Additional tests of urethral perfusion with PGE2 were made. PGE2 decreased bladder capacity, increased voiding efficiency, and increased sphincter EMG during open cystometry compared with saline controls. The number of nonvoiding contractions did not change with PGE2; however, bladder compliance decreased. During closed-outlet cystometry, PGE2 applied only to the bladder or the urethra did not decrease bladder capacity. Urethral infusion of PGE2 decreased urethral perfusion pressure. Taken together, these results suggest that intravesical PGE2 may decrease bladder capacity by targeting afferents in the proximal urethra. This may occur through urethral relaxation and decreased bladder compliance, both of which may increase activation of proximal urethra afferents from distension of the proximal urethra. This hypothesis stands in contrast to many hypotheses of urgency that focus on bladder dysfunction as the primary cause of OAB symptoms. Targeting the urethra, particularly urethral smooth muscle, may be a promising avenue for the design of drugs and devices to treat OAB.
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Registered trials
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.