Aim:The etiology of the ejaculatory disorder induced by alpha-1 blockers is still controversial, although it has been suggested to be retrograde ejaculation. The aim of this study was to investigate the distribution of alpha-1 adrenoceptor subtype mRNA in human seminal vesicles, and to analyze the prevalence and etiology of the disorder in healthy men. Methods: Experimental Study. Seminal vesicles from 10 surgical specimens (eight radical prostatectomy, two radical cystectomy) were dissected. Real-time PCR was conducted for quantification of mRNA expression of each alpha-1 adrenoceptor subtype. Clinical Study. Ejaculatory disorder was investigated using 17 healthy male volunteers. Tamsulosin (0.2 mg and 0.4 mg) and naftopidil (50 mg and 100 mg) were administered in a crossover manner for 3 days. The ejaculatory volume, sperm count in midstream urine after ejaculation, and fructose concentration in seminal plasma were investigated. Results: Real-time PCR revealed that alpha-1a mRNA was significantly predominant in seminal vesicles (P < 0.001; 1a, 75.0%; 1b, 11.7%; 1d, 13.3%). Ejaculatory volume (baseline 2.72 ± 0.28 mL) significantly decreased in the tamsulosin group (0.2 mg, 1.75 ± 0.31 mL; 0.4 mg, 1.51 ± 0.39 mL; P < 0.05), but not in the naftopidil group (50 mg, 2.70 ± 0.24 mL; 100 mg, 2.48 ± 0.26 mL; P = NS). There was no sperm in midstream urine after any ejaculation. Conclusions: The current study demonstrates that alpha-1a mRNA is predominant among the adrenoceptor subtypes in human seminal vesicles. Decreased capacity of contraction of the seminal vesicles is proposed as the cause of the ejaculatory disorder induced by alpha-1 blockers.

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Introduction Recent studies have highlighted the influence of α1-adrenoceptor antagonists on ejaculatory function. Aim We evaluated the effect of a new, highly selective α1A-blocker, silodosin, on ejaculatory function of normal volunteers. Methods The study included 15 healthy male urologists who voluntarily participated in the study. They took 4 mg of silodosin or a placebo twice daily for 3 days in a randomized, double-blind crossover design. Main Outcome Measures We investigated the ejaculatory volume, sperm count in urine after ejaculation, and fructose concentration in seminal plasma before and after administration of the agents. Results All volunteers on silodosin had a complete lack of ejaculation. Three days after completion of silodosin, the mean ejaculatory volume recovered to the baseline level. There was no sperm in urine after ejaculation under silodosin administration in any volunteer. Conclusions All volunteers on silodosin had anejaculation and did not show post-ejaculate sperm in their urine. The mechanism of ejaculatory dysfunction caused by silodosin is a loss of seminal emission.

Introduction The bed nucleus of the stria terminalis (BNST) exhibits several sex differences that may be related to male sexual behavior and gender identity. In mice and rats, sex differences in the principal nucleus of the BNST (BNSTp) are due to sexually dimorphic cell death during perinatal life. Although testosterone treatment of newborn female rats increases BNSTp cell number, the relevant hormone metabolite(s) are not known, and the effect of testosterone on the development of BNSTp cell number in mice has not been examined. Aim To identify the sex hormone metabolites and receptors controlling cell number, volume, and cell size in the BNSTp of mice. Methods In the first experiment, C57BL/6J male mice were injected on the day of birth with peanut oil; females were injected with testosterone propionate (TP), estradiol benzoate (EB), dihydrotestosterone propionate (DHTP), or oil alone, and the BNSTp of all animals was examined in adulthood. In the second experiment, to compare effects of EB to the effects of estrogen receptor subtype specific agonists, newborn female mice were injected with EB, propyl-pyrazole-triol (PPT, a selective estrogen receptor alpha [ERα] agonist), or diarylpropionitrile (DPN, a selective estrogen receptor beta [ERβ] agonist). Main Outcome Measures Nuclear volume measurements and stereological cell counts in the BNSTp in adulthood. Results TP treatment of newborn females completely masculinized both BNSTp volume and cell number. EB masculinized neuron number, whereas DHTP had no effect on volume or cell number. In the second experiment, EB again fully masculinized neuron number in the BNSTp and in this study also masculinized BNSTp volume. PPT and DPN each significantly increased cell number, but neither completely mimicked the effects of EB. Conclusions We conclude that estrogenic metabolites of testosterone control sexually dimorphic cell survival in the BNSTp and that activation of both ERα and ERβ may be required for complete masculinization of this brain region.