title: Effects of beta antagonists on mechanical properties in rabbit ciliary artery.
abstract: BACKGROUND
  We set out to clarify the mechanisms involved in the effectiveness of beta-adrenergic receptor antagonists on the ocular circulation.
  
  
  METHODS
  The effects of three beta antagonists, timolol, betaxolol and carteolol, on the isolated rabbit ciliary artery were investigated in vitro using isometric tension recording methods.
  
  
  RESULTS
  Phenylephrine dose-dependently contracted ciliary artery smooth muscle, and bunazosin (1 microM) shifted this dose-response curve to the right. Isoproterenol, on the other hand, had no effect up to the concentration of 1 mM. Betaxolol and timolol had no effect on the ciliary artery. However, carteolol dose-dependently contracted this muscle from a concentration of 1 microM. After precontraction by excess-[K]0 solutions, application of betaxolol or timolol dose-dependently provoked relaxation; the minimum concentration of betaxolol or timolol required to generate the relaxation was 100 microM and 300 microM, respectively. Carteolol did not generate relaxation at concentrations up to 1 mM. After pretreatment with L-NAME (300 microM), the amplitude of relaxation induced by 10 microM carbachol was reduced to 33.0+/-20.2%, while betaxolol- or timolol-induced relaxation was unchanged. Diltiazem (10 microM) induced relaxation which was not inhibited by pretreatment with L-NAME.
  
  
  CONCLUSIONS
  Betaxolol and timolol could directly relax rabbit ciliary artery in vitro at relatively high concentrations, and relaxation was not due to NO released from the preparation. Presumably, this relaxation occurs through action similar to Ca antagonists. However, the clinical importance of this effect is not yet clear. Carteolol had no relaxant effect in vitro.
authors.affiliation: Department of Ophthalmology, Kitasato University School of Medicine, Kitasato University, Kanagawa, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Hayashi-Morimoto
authors.forename: T
authors.initials: T
authors.lastname: Yoshitomi
authors.forename: H
authors.initials: H
authors.lastname: Ishikawa
authors.forename: E
authors.initials: E
authors.lastname: Hayashi
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D015784:Betaxolol / Q000494:pharmacology*; D002354:Carteolol / Q000494:pharmacology*; D018679:Cholinergic Agonists / Q000494:pharmacology; D019842:Ciliary Arteries / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D010656:Phenylephrine / Q000494:pharmacology; D011817:Rabbits; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D013999:Timolol / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D018679:Cholinergic Agonists; D004791:Enzyme Inhibitors; D018340:Receptors, Adrenergic, alpha-1; D010656:Phenylephrine; D013999:Timolol; D002354:Carteolol; D007545:Isoproterenol; D015784:Betaxolol