Objectives
To investigate the mechanism underlying the ameliorating effect of tamsulosin, an α
1-adrenoceptor antagonist, on storage symptoms associated with benign prostatic hyperplasia, the effects of tamsulosin on bladder blood flow (BBF) and bladder function was evaluated in rats with bladder outlet obstruction (BOO).
Methods
BOO was produced by partial ligature of the proximal urethra, which was maintained for 2 weeks. Tamsulosin was subcutaneously administered via an osmotic pump for 2 weeks immediately after the BOO surgery. The BBF in the sham-operated rats, the control BOO rats, and the tamsulosin-treated BOO rats was measured using the fluoromicrosphere method. Each rat was kept in a metabolic cage for observation of micturition behavior. Expression of the α1-adrenoceptor subtype mRNA in the vesical artery was measured by reverse transcriptase-polymerase chain reaction.
Results
BBF was significantly reduced in BOO rats compared with sham-operated rats, and tamsulosin significantly increased the BBF in BOO rats. Tamsulosin ameliorated the decrease in mean voided volume in BOO rats with bladder masses < 500 mg. Expression of the α1-adrenoceptor subtype in the vesical artery was α1a- > α1d-adrenoceptors; almost no expression was observed of α1b-adrenoceptors in either sham-operated or BOO rats.
Conclusions
Tamsulosin increased BBF in BOO rats via an antagonistic effect, presumably on the α1A- and/or α1D-adrenoceptor in the vesical artery mainly, and improved the decrease in mean voided volume. Therefore, the results of this study suggest that tamsulosin improves bladder overactivity via improvement of BBF.
