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Background  To investigate the effect of prostaglandin depletion by means of COX-inhibition on cholinergic enhanced spontaneous contractions.    Methods  The urethra and bladder of 9 male guinea pigs (weight 270–300 g) were removed and placed in an organ bath with Krebs’ solution. A catheter was passed through the urethra through which the intravesical pressure was measured. The muscarinic agonist arecaidine, the non-selective COX inhibitor indomethacin, and PGE 2  were subsequently added to the organ bath. The initial average frequency and amplitude of spontaneous contractions in the first 2 minutes after arecaidine application were labelled F ini  and P ini , respectively. The steady state frequency (F steady ) and amplitude (P steady ) were defined as the average frequency and amplitude during the 5 minutes before the next wash out.    Results  Application of 1 μM PGE 2  increased the amplitude of spontaneous contractions without affecting frequency. 10 μM of indomethacin reduced amplitude but not frequency.  The addition of indomethacin did not alter F ini  after the first application (p = 0.7665). However, after the second wash, F ini  was decreased (p = 0.0005). F steady , P steady  and P ini  were not significantly different in any of the conditions. These effects of indomethacin were reversible by PGE 2  addition. .Conclusions  Blocking PG synthesis decreased the cholinergically stimulated autonomous contractions in the isolated bladder. This suggests that PG could modify normal cholinergically evoked response. A combination of drugs inhibiting muscarinic receptors and PG function or production can then become an interesting focus of research on a treatment for overactive bladder syndrome.

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder