title: Comparison of prazosin, terazosin and tamsulosin: functional and binding studies in isolated prostatic and vascular human tissues.
abstract: BACKGROUND
  Terazosin and tamsulosin are drugs currently used in the treatment of benign prostatic hypertrophy (BPH). The potency of these two alpha(1) receptor antagonists and that of prazosin to inhibit contractions induced by noradrenaline and the binding of [(3)H]-prazosin in human prostate and four different human arterial and venous vessels (saphenous and umbilical veins, renal and mesenteric arteries) was studied.
  
  
  METHODS
  By bioassay and binding studies, we examined the receptor affinities of different alpha(1) receptor antagonists in different human tissues.
  
  
  RESULTS
  pKb of terazosin, tamsulosin, and prazosin obtained in the prostatic tissues (8.15, 9.64, and 8.59, respectively) were not different from those obtained in the umbilical veins (8.07, 9.56, and 8.30, respectively), in the mesenteric artery (8.27, 10.29, and 9.01, respectively), renal artery (8.35, 10.13, and 8.76, respectively) and saphenous vein (7.8, 10.3, and 9.32, respectively). IC(50) (nM) of prazosin, terazosin, and tamsulosin obtained from binding studies in membrane preparations from prostate tissue were similar to those from umbilical veins, saphenous vein, and renal artery.
  
  
  CONCLUSIONS
  All of the evaluated drugs showed similar selectivity for prostatic vs. vascular tissues. Thus, different clinical profiles of the present drugs should not result from their differential affinity for prostatic versus vascular alpha(1)-adrenoceptors.
authors.affiliation: Department of Experimental and Clinical Medicine, Pharmacology Unit, University of Ferrara, Ferrara, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Amadesi
authors.forename: K
authors.initials: K
authors.lastname: Varani
authors.forename: L
authors.initials: L
authors.lastname: Spisani
authors.forename: C
authors.initials: C
authors.lastname: Daniele
authors.forename: A
authors.initials: A
authors.lastname: Turini
authors.forename: G
authors.initials: G
authors.lastname: Agnello
authors.forename: P
authors.initials: P
authors.lastname: Zamboni
authors.forename: P A
authors.initials: PA
authors.lastname: Borea
authors.forename: P
authors.initials: P
authors.lastname: Geppetti
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000378:metabolism / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D011224:Prazosin / Q000031:analogs & derivatives / Q000378:metabolism / Q000494:pharmacology; D011467:Prostate / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism / Q000502:physiology; D012077:Renal Artery / Q000187:drug effects; D012501:Saphenous Vein / Q000187:drug effects; D013449:Sulfonamides / Q000378:metabolism / Q000494:pharmacology; D000077409:Tamsulosin; D014471:Umbilical Veins / Q000187:drug effects
chemical_list: D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D013449:Sulfonamides; C041226:Terazosin; D000077409:Tamsulosin; D009638:Norepinephrine; D011224:Prazosin