title: Roles of nitric oxide and prostacyclin in triethyleneglycol dimethacrylate (TEGDMA)-induced vasorelaxation.
abstract: OBJECTIVE
  Most dental resinous materials contain the diluent monomer triethyleneglycol dimethacrylate (TEGDMA), which has been reported to be bioactive. Previously, it was demonstrated that TEGDMA induces vasorelaxation. The present study examines the mechanism(s) of the TEGDMA-induced vasorelaxation by measuring vascular nitrite and prostacyclin levels.
  
  
  METHODS
  Nitrite and prostacyclin levels were assayed in rat aortic tissues in response to TEGDMA. The involvement of guanylyl and adenylyl cyclases in TEGDMA-induced aortic vasorelaxation was determined using the enzyme inhibitors 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (SQ22536), respectively.
  
  
  RESULTS
  TEGDMA enhanced the levels of nitrites in endothelium-intact and that of protacyclin in both endothelium-intact and denuded rat aortas. The increase in nitrites was associated with endothelium-dependent aortic relaxation mediated via the activation of guanylyl cyclase, while the increase in prostacyclin was associated with both endothelium-dependent and independent relaxation linked to adenylyl cyclase stimulation.
  
  
  CONCLUSIONS
  Data from the present investigation can be relevant to dental practice employing materials containing TEGDMA by providing insights into the vasorelaxant effect of the monomer following placement of the materials in the oral cavity. Additional studies that are more relevant to the clinical situation are required to confirm these initial results and further explore their implications.
authors.affiliation: Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, CL-2130, Medical College of Georgia, Augusta, GA 30912-1128, USA. wabebe@mail.mcg.edu
authors.forename: Worku
authors.initials: W
authors.lastname: Abebe
authors.forename: William F
authors.initials: WF
authors.lastname: Maddux
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives / Q000494:pharmacology; D000067956:Adenylyl Cyclase Inhibitors; D000262:Adenylyl Cyclases / Q000502:physiology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000378:metabolism; D003188:Composite Resins / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D011464:Epoprostenol / Q000032:analysis / Q000502:physiology*; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors / Q000502:physiology; D008297:Male; D009569:Nitric Oxide / Q000032:analysis / Q000502:physiology*; D009573:Nitrites / Q000032:analysis; D010069:Oxadiazoles / Q000494:pharmacology; D011092:Polyethylene Glycols / Q000008:administration & dosage / Q000494:pharmacology*; D011109:Polymethacrylic Acids / Q000008:administration & dosage / Q000494:pharmacology*; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D011921:Rats, Inbred WKY; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: C095284:1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one; D000067956:Adenylyl Cyclase Inhibitors; D003188:Composite Resins; D004791:Enzyme Inhibitors; D009573:Nitrites; D010069:Oxadiazoles; D011109:Polymethacrylic Acids; D011810:Quinoxalines; D014665:Vasodilator Agents; C020946:triethylene glycol dimethacrylate; C017759:9-(tetrahydro-2-furyl)-adenine; D009569:Nitric Oxide; D011092:Polyethylene Glycols; D011464:Epoprostenol; D000262:Adenylyl Cyclases; D006162:Guanylate Cyclase; D000225:Adenine