title: Ejaculatory disorder caused by alpha-1 adrenoceptor antagonists is not retrograde ejaculation but a loss of seminal emission.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Urology, School of Medicine, Sapporo Medical University, Sapporo, Hokkaido, Japan. hisasue@sapmed.ac.jp
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Hisasue
authors.forename: Ryoji
authors.initials: R
authors.lastname: Furuya
authors.forename: Naoki
authors.initials: N
authors.lastname: Itoh
authors.forename: Ko
authors.initials: K
authors.lastname: Kobayashi
authors.forename: Seiji
authors.initials: S
authors.lastname: Furuya
authors.forename: Taiji
authors.initials: T
authors.lastname: Tsukamoto
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000009:adverse effects*; D000328:Adult; D000368:Aged; D004542:Ejaculation / Q000187:drug effects*; D005500:Follow-Up Studies; D015870:Gene Expression; D006801:Humans; D008297:Male; D008875:Middle Aged; D009281:Naphthalenes / Q000009:adverse effects; D010879:Piperazines / Q000009:adverse effects; D012333:RNA, Messenger / Q000235:genetics; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012661:Semen / Q000187:drug effects / Q000378:metabolism; D012735:Sexual Dysfunction, Physiological / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D013449:Sulfonamides / Q000009:adverse effects; D000077409:Tamsulosin
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D009281:Naphthalenes; D010879:Piperazines; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D013449:Sulfonamides; D000077409:Tamsulosin; C064357:naftopidil