Serotonin(5-HT): can it be a cause in overactive bladder

Kim, Hyung Jee; Lee, Suk Jae

Abstract

PURPOSE
The purpose of this study is to investigate in vitro the effects of serotonin on the rat detrusor. In particular, this study examines what drugs inhibit the serotonin-induced detrusor contractions.
MATERIALS AND METHODS
Isometric tension changes of isolated rat bladder muscle strips were recorded in an organ bath using a force transducer. Acute effects of serotonin (0.0001-0.01mM) were assessed on resting tension. Electrical field stimulation (EFS), bethanechol (0.0001-0.01mM), ATP (1-3mM) or KCl(63.5-254mM)-induced contractions using application in organ bath were compared with serotonin-induced contractions. In order to examine the action mechanism of serotonin-induced stimulation, EFS, bethanechol, ATP or KCl-induced contraction under serotonin (0.001mM) was assessed and serotonin (0.001 to 0.1mM) was cumulatively added to the organ bath following pre-incubation with propranolol, ketanserine, tropisetron, propiverine, sodium nitroprusside or doxazocin.
RESULTS
There are two phases to the serotonin-induced responsean initial transient contraction and a prolonged tonic phase. Serotonin produced a reversible and dose-dependent contraction of the detrusor strips. Responses to bethanechol significantly increased with a concentration of 0.001mM serotonin (p<0.05). There was no effect on the responses to ATP, KCl, or EFS under 0.001mM serotonin. The 5-HT2 receptor is mainly responsible for serotonin-induced contractions of the detrusor (p<0.05), while the 5-HT1 receptor is partially responsible. Doxazocin and propiverine each significantly suppressed the responses to serotonin, while sodium nitroprusside and tropisetron each had no effect (p<0.05).
CONCLUSIONS
Because the 5-HT2 antagonist blocked the effect of serotonin-induced bladder contractions and the stimulation of the adrenoreceptors, the 5-HT2 antagonist seems to improve lower urinary tract symptoms.