title: Prostatic inflammation and obstructive voiding in the adult Noble rat: impact of the testosterone to estradiol ratio in serum.
abstract: BACKGROUND
  The age-related decline of the testosterone to estradiol (T-to-E(2)) ratio in serum is associated with the increased prevalence of prostatic inflammation and lower urinary tract symptoms suggesting obstructive voiding. The impact of the T-to-E(2) ratio on the development and reversal of non-bacterial prostatic inflammation and obstructive voiding was tested in adult Noble rats.
  
  
  METHODS
  Adult male Noble rats (n = 16) were treated with estradiol (83 microg/day) and two different doses (280 and 830 microg/day) of testosterone to cause hypoandrogenic and hyperandrogenic states with elevated estrogen. After the 13-week hormonal treatment, urodynamical measurements and electrical activity recording of the rhabdosphincter muscle were performed under anesthesia. Testosterone, estradiol, and prolactin concentrations in serum were measured and inflammatory changes in the dorsolateral prostate were classified and counted.
  
  
  RESULTS
  Histopathological and urodynamical analyses indicated that the hypoandrogenic animals with a decreased T-to-E(2) ratio (10 versus > 300 in control) developed prostatic inflammation and non-obstructive voiding. The hyperandrogenic state with decreased T-to-E(2) ratio of 50 decreased the aggressiveness of the inflammation and the number of inflamed acini in the prostate and caused urethral obstruction associated with rhabdosphincter dysfunction.
  
  
  CONCLUSIONS
  Different responses of the prostatic inflammation and voiding function to the change in T-to-E(2) ratio imply that non-bacterial prostatic inflammation is not a sufficient condition for the development of obstructive voiding. The present study finds no support for the idea that age- and/or obesity-related hypoandrogenic state with a decreased ratio of T-to-E(2) would cause urethral obstruction.
authors.affiliation: Institute of Biomedicine, Department of Anatomy, University of Turku, Turku, Finland. jenni.bernoulli@utu.fi
authors.forename: Jenni
authors.initials: J
authors.lastname: Bernoulli
authors.forename: Emrah
authors.initials: E
authors.lastname: Yatkin
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Konkol
authors.forename: Eva-Maria
authors.initials: EM
authors.lastname: Talvitie
authors.forename: Risto
authors.initials: R
authors.lastname: Santti
authors.forename: Tomi
authors.initials: T
authors.lastname: Streng
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000097:blood* / Q000502:physiology; D008297:Male; D009929:Organ Size; D011388:Prolactin / Q000097:blood; D011467:Prostate / Q000473:pathology; D011472:Prostatitis / Q000097:blood* / Q000209:etiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013739:Testosterone / Q000097:blood* / Q000502:physiology; D014524:Urethral Obstruction / Q000097:blood* / Q000209:etiology*; D014554:Urination / Q000187:drug effects / Q000502:physiology
chemical_list: D013739:Testosterone; D004958:Estradiol; D011388:Prolactin