| Autor: |
Tatemichi, Satoshi, Akiyama, Katsuyoshi, Kobayashi, Mamoru, Yamazaki, Yoshinobu, Yokoyama, Osamu, Uruno, Tsutomu |
| Předmět: |
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| Zdroj: |
Journal of Urology; Sep2006, Vol. 176 Issue 3, p1236-1241, 6p |
| Abstrakt: |
Purpose: α1-Adrenoceptor antagonists relax the obstructed prostatic urethra and suppress the irritative symptoms frequently observed in patients with benign prostatic hyperplasia. We investigated the effects of 3 α1-adrenoceptor antagonists on urodynamics in rats with hormone induced benign prostatic hyperplasia to determine which α1-adrenoceptor subtype selective antagonists would suppress irritative symptoms. Materials and Methods: Rats were treated with testosterone and 17β-estradiol by weekly intramuscular injections. After 4 weeks a pressure flow study was done and the effects of the α1-adrenoceptor antagonists KMD-3213 silodosin, tamsulosin and prazosin on urodynamics were compared. We especially investigated the involvement of the bladder and prostatic urethra to clarify the mechanism of detrusor overactivity expression. Results: Hormone treatment induced benign prostatic hyperplasia and resulted in detrusor overactivity, as determined by cystometry. Baseline perfusion urethral pressure and the phenylephrine induced increase in it were significantly higher in rats with vs without benign prostatic hyperplasia. Cystometry in hormone treated female rats did not show detrusor overactivity. KMD-3213 decreased detrusor overactivity, similar to other α1-adrenoceptor antagonists. Conclusions: These results suggest that an excessive response to sympathetic nerve stimulation, which is mainly mediated via α1A-adrenoceptor, in the hypertrophied prostate gives rise to detrusor overactivity. Furthermore, the α1A-adrenoceptor selective antagonist KMD-3213 would be suitable for improving irritative symptoms in patients with benign prostatic hyperplasia. [Copyright &y& Elsevier] |
| Databáze: |
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