Inhibition by tamsulosin of tension responses of human hyperplastic prostate to electrical field stimulation

Tamsulosin (10^-10-10^-9 M) or prazosin (10^-9-10^-8 M) concentration dependently blocked the tension responses to electrical field stimulation (0.3 ms duration, 80 V and 20 Hz) in human hyperplastic prostate with IC₅₀ values of (1.93 ± 0.26) x 10^-10 M and (2.11 ± 0.21) x 10^-9 M, respectively. The relative potency of tamulosin with reference to prazosin was 10.96. The pA₂ values for tamulosin and prazosin against phenylephrine-induced contractions were 10.05 ± 0.16 and 9.25 ± 0.07, respectively. The relative potency of tamsulosin with reference to prazosin was 6.31. In the presence of prazosin to block α₁-adrenoceptor-mediated responses, nifedipine (10^-5 M), but not tamsulosin (10^-9 M), significantly blocked the tension responses in human hyperplastic prostate induced by increasing [Ca²⁺](o) concentrations (10^-4 to 3 x 10^-3 M) in a Ca²⁺-free environment pre-depolarized with 60 mM K⁺. Additionally, the effects of prazosin and tamsulosin on electrical field stimulation-evoked [³H]noradrenaline release were studied on the S₃/S₂ ratios. It appeared that both drugs had little effect on this release reaction, with S₃/S₂ ratios of 0.96 ± 0.02 and 0.90 ± 0.02, respectively. These results indicate that tamsulosin is a potent antagonist against endogenous sympathetic stimulation in human hyperplastic prostate.