Antimuscarinic Drug Inhibits Detrusor Overactivity Induced by Topical Application of Prostaglandin E2 to the Urethra With a Decrease in Urethral Pressure

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Antimuscarinic drugs increase bladder capacity without prominent side effects such as urinary retention even when administered to patients with mild to moderate bladder outlet obstruction. Some mechanisms might exist in the urethra to compensate for the emptying function of the detrusor after the administration of antimuscarinic drugs. We investigated the influence of the antimuscarinic drug propiverine (Taiho Pharmaceutical, Tokyo, Japan) on urethral function.

Materials and Methods

Urethral pressure and rhythmic bladder pressure were simultaneously monitored in urethane anesthetized female Sprague-Dawley rats. Prostaglandin E2 was continuously administered intravesically or intraurethrally to induce detrusor overactivity. To eliminate the influence of bladder activity and monitor urethral baseline pressure isovolumetric pressure of the urethra was then recorded after cystectomy and ligation of the external urethral meatus. Furthermore, in vitro contractile responses of the urethral circular smooth muscle to field stimulation were examined in the presence of propiverine, tamsulosin (Taiho Pharmaceutical), verapamil, ω-conotoxin and atropine (Sigma®).


Intravesical or intraurethral administration of prostaglandin E2 significantly decreased the bladder contraction interval by 10.7% and 36.0%, respectively. Intra-arterial administration of 2 × 102 nM/kg propiverine significantly increased the bladder contraction interval in rats receiving intraurethral prostaglandin E2 by 81.8% but it had no marked effect on rats receiving intravesical prostaglandin E2. Significant decreases in urethral baseline pressure were found after propiverine administration. Field stimulation induced contraction was inhibited by propiverine and verapamil but not by tamsulosin, ω-conotoxin or atropine.


These results suggest that the inhibitory effects of propiverine are more prominent in rats with detrusor overactivity induced by intraurethral prostaglandin E2 than by intravesical prostaglandin E2. Propiverine may compensate for detrusor function by decreasing urethral resistance in the voiding phase.

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