title: Gene expressions and mechanical functions of α1-adrenoceptor subtypes in mouse ureter.
abstract: OBJECTIVE
  This study was performed to characterize the α1-adrenoceptor subtypes in mouse ureters as regards gene expressions and contractile functions.
  
  
  METHODS
  The mRNAs for these subtypes were quantified by the real-time quantitative reverse transcription polymerase chain reaction. In a functional study, α1-adrenoceptor antagonists were evaluated against the noradrenaline-induced contraction in mouse isolated ureteral preparations.
  
  
  RESULTS
  In mouse ureter, the relative mRNA expression levels for α1a-, α1b- and α1d-adrenoceptors were 74.5, 14.3 and 11.2%, respectively. Adrenaline and noradrenaline each produced a concentration-dependent phasic contraction (pD 2 values, 5.73±0.05 and 5.69±0.06, respectively). Prazosin (non-selective α1-adrenoceptor antagonist), silodosin (selective α1A-adrenoceptor antagonist), and BMY-7378 (selective α1D-adrenoceptor antagonist) all shifted the concentration–response curve for noradrenaline to the right, the rank order of potencies (apparent pA 2 values) being silodosin (9.32±0.11)>prazosin (8.55±0.10)>BMY-7378 (6.06±0.15). The α1A-adrenoceptor antagonist silodosin was thus much more effective than the α1D-adrenoceptor antagonist BYM-7378.
  
  
  CONCLUSIONS
  Our results demonstrate that in mouse ureters: the mRNA for the α1A-adrenoceptor was more prevalent than those for the α1B- and α1D-adrenoceptors, and that among these subtypes, the α1A-adrenoceptor plays the major role in noradrenaline-induced contraction.
authors.affiliation: Pharmacology, Research and Development, Kissei Pharmaceutical Co. Ltd., 4365-1, Kashiwabara, Hotaka, Azumino, Nagano 399-8304, Japan. shinya_kobayashi@pharm.kissei.co.jp
authors.forename: Shinya
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Tomiyama
authors.forename: Yuji
authors.initials: Y
authors.lastname: Hoyano
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Yamazaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kusama
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Itoh
authors.forename: Yasue
authors.initials: Y
authors.lastname: Kubota
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kohri
mesh_terms: D058668:Adrenergic alpha-1 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D004837:Epinephrine / Q000494:pharmacology; D015870:Gene Expression / Q000502:physiology; D007211:Indoles / Q000494:pharmacology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics* / Q000502:physiology*; D014513:Ureter / Q000187:drug effects / Q000502:physiology*
chemical_list: C547714:Adra1a protein, mouse; C547717:Adra1b protein, mouse; C547720:Adra1d protein, mouse; D058668:Adrenergic alpha-1 Receptor Antagonists; D007211:Indoles; D010879:Piperazines; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; C095285:silodosin; C053428:BMY 7378; D009638:Norepinephrine; D011224:Prazosin; D004837:Epinephrine