Related Experiment Video
Updated: Feb 25, 2026
07:42
Nerve-sparing Mid-urethral Obstruction NeMO in Female Small Rodents
Published on: April 25, 2017
10.1K
OAB without an overactive bladder in the acute prostaglandin E2 rat model.
James A Hokanson1, Christopher L Langdale1, Arun Sridhar2
1Department of Biomedical Engineering, Duke University, Durham, North Carolina.
American Journal of Physiology. Renal Physiology
|August 4, 2017
Summary
Prostaglandin E2 (PGE2) reduces bladder capacity by affecting the urethra, not the bladder itself. This suggests targeting urethral smooth muscle may treat overactive bladder (OAB) symptoms.
Area of Science:
- Urology
- Pharmacology
- Physiology
Background:
- Intravesical prostaglandin E2 (PGE2) is known to induce overactive bladder (OAB) symptoms.
- PGE2 reduces bladder capacity in rats and causes urgency in humans.
- The precise mechanism of PGE2-induced OAB symptoms remains unclear.
Purpose of the Study:
- To elucidate the mechanism by which intravesical PGE2 reduces bladder capacity.
- To investigate the role of the urethra and bladder in PGE2's effect on bladder capacity.
Main Methods:
- Single-fill cystometry with simultaneous sphincter electromyography (EMG) in urethane-anesthetized rats.
- Selective intravesical or urethral administration of PGE2 using closed-outlet cystometry.
- Urethral perfusion pressure measurements.
Main Results:
- Intravesical PGE2 decreased bladder capacity, increased voiding efficiency, and increased sphincter EMG.
- PGE2 decreased bladder compliance but did not alter nonvoiding contractions.
- Selective application of PGE2 to the bladder or urethra did not reduce capacity; urethral PGE2 infusion decreased urethral perfusion pressure.
Conclusions:
- Intravesical PGE2 likely reduces bladder capacity by targeting afferents in the proximal urethra.
- Urethral relaxation and decreased bladder compliance may increase proximal urethral afferent activation.
- Targeting urethral smooth muscle could be a novel strategy for treating OAB.
