title: Pharmacological properties of serotonin receptor subtypes mediating contraction of bovine inferior alveolar arteries.
abstract: OBJECTIVE
  To characterise the 5-hydroxytryptamine (5-HT) receptor subtypes mediating contraction of the inferior alveolar artery. Additionally, to determine the role of cyclooxygenase products, nitric oxide, endothelium, monoamine oxidase and 5-HT uptake in modulating contraction of inferior alveolar arteries to 5-HT.
  
  
  METHODS
  Contractile responses to 5-HT were examined in vitro using ring segments of bovine inferior alveolar arteries. Affinity constants (K(B)'s) of subtype-selective 5-HT receptor antagonists were determined to characterise the 5-HT receptor-subtypes causing contraction of inferior alveolar arteries.
  
  
  RESULTS
  In 100 nM ketanserin or 30 nM spiperone, 5-HT caused a biphasic contraction best-fit by a two-site curve model, where one site was antagonist-sensitive and the other site antagonist-insensitive. 5-HT(2A) receptor-subtype selective antagonists, ketanserin and spiperone, blocked 5-HT induced contraction with K(B)'s of 1.0 and 0.16 nM, respectively. RS102221 (5-HT(2C) selective) and (S)-WAY100135 (5-HT(1A) selective) blocked 5-HT stimulated contraction with low affinities (K(B)'s=100 nM and 330 nM, respectively). GR55562, a 5-HT(1) receptor subtype antagonist with a reported affinity of 500 nM at the 5-HT(1D) receptor subtype, blocked 5-HT induced contraction with a K(B) of 470 nM. Cylooxygenase inhibition with 50 microM ibuprofen caused a 44% increase in maximal contraction to 5-HT; whereas, nitric oxide inhibition with N(G)-nitro-L-arginine, endothelium removal or inhibition of 5-HT uptake and monoamine oxidase with imipramine and iproniazid, respectively, did not affect 5-HT contraction.
  
  
  CONCLUSIONS
  Both 5-HT(2A) and 5-HT(1D/1B) receptor subtypes mediate 5-HT induced contraction of the bovine inferior alveolar artery. 5-HT stimulated contraction of the inferior alveolar artery is modulated by a vasodilator prostaglandin.
authors.affiliation: Department of Pharmacology, Creighton University School of Medicine, Criss III, Room 553, 2500 California Plaza, Omaha, NE 68178, USA.
authors.forename: H A
authors.initials: HA
authors.lastname: O'Donohue
authors.forename: P W
authors.initials: PW
authors.lastname: Abel
authors.forename: C S
authors.initials: CS
authors.lastname: Bockman
mesh_terms: D000539:Alveolar Process / Q000098:blood supply*; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000502:physiology; D002417:Cattle; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000502:physiology; D007650:Ketanserin / Q000494:pharmacology; D008334:Mandible / Q000098:blood supply; D011985:Receptors, Serotonin / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology; D012702:Serotonin Antagonists / Q000494:pharmacology*; D013134:Spiperone / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology
chemical_list: D011985:Receptors, Serotonin; D012702:Serotonin Antagonists; D012701:Serotonin; D013134:Spiperone; D007650:Ketanserin