Vasodilatory Effect of Hydroxyethyl Methacrylate and Triethylene Glycol Dimethacrylate in Rat Aorta through Calcium Antagonistic Action

Guven G., Seyrek M., Vural I. M., ÇEHRELİ Z. C., Yildiz O.

JOURNAL OF ENDODONTICS, vol.37, no.3, pp.353-357, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 37 Issue: 3
  • Publication Date: 2011
  • Doi Number: 10.1016/j.joen.2010.11.038
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.353-357
  • Hacettepe University Affiliated: Yes


Introduction: Resin-based dental materials contain various diluent monomers that can interfere with vascular function by causing vasodilation. In this study, we evaluated the vasoactive potential of hydroxyethyl methacrylate (HEMA) and triethylene glycol dimethacrylate (TEGDMA) and the possible mechanism of their vascular action on isolated rat aorta. Methods: Responses of thoracic aorta rings were recorded isometrically by using force displacement transducers. After precontracting aorta rings with phenylephrine, relaxations to HEMA and TEGDMA were recorded in the absence and presence of nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester, cyclooxygenase inhibitor indomethacin,, and K+ channel inhibitors tetraethylammonium, glibenclamide, and 4-aminopyridine. To investigate the Ca2+-channel antagonistic effect of HEMA and TEGDMA in different aorta rings, concentration-response curves to CaCl2 were obtained in the absence and presence of the test monomers. Results: Both HEMA and TEGDMA elicited concentration-dependent relaxations. The vasorelaxant effect of HEMA and TEGDMA was not mediated via endothelium-dependent nitric oxide and prostanoid-dependent mechanisms or by K+ efflux through K+ channels. Both monomers significantly inhibited the contractions induced by CaCl2. Conclusions: Our results showed that HEMA and TEGDMA induce vasodilation via Ca2+-antagonistic action, whereas nitric oxide and cyclooxgenase pathway and K+ channels were not responsible for this vasoactive effect. (J Endod 2011;37:353-357)