The Vasorelaxant Effect of HEMA and TEGDMA Through Calcium-Antagonistic Action

OBJECTIVES: Resin-based dental materials contain various diluent monomers that can interfere with vascular function by causing vasorelaxation. In this study, we evaluated the vasoactive potential of hydroxyethyl methacrylate (HEMA) and triethylene glycol dimethacrylate (TEGDMA), and the possible mechanism(s) of their vascular action on isolated rat aorta. METHODS: Responses of thoracic rat aorta rings were recorded isometrically by using force displacement transducers. After pre-contracting aorta rings, relaxations to HEMA and TEGDMA were recorded in the absence and presence of nitric oxide synthase inhibitor Nù-nitro-L-arginine methyl ester(L-NAME), cyclooxygenase inhibitor indomethacin, and K+ channel inhibitors: tetraethylammonium(TEA), glibenclamide(GLI) and 4-aminopyridine(4-AP). 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. Comparison among multiple groups were made by using One-way ANOVA, followed by post-hoc Scheffe's test to determine significant differences among the means of the data groups. Comparisons between two groups were made by using Mann- Whitney U test. P<0.05 was accepted as significant difference. RESULTS: Both HEMA and TEGDMA elicited concentration-dependent relaxations. The vasorelaxant effect of HEMA and TEGDMA was not inhibited by L-NAME and indomethacin. Likewise, relaxation to TEGDMA and HEMA was not significantly modified by incubation of aorta with the K channel inhibitors TEA, 4-AP or GLI. Both monomers significantly inhibited the contractions induced by CaCl2. CONCLUSION: Our results show that HEMA and TEGDMA induce vasorelaxation responses via Ca2+-antagonistic action, while NO and cyclooxgenase pathway and K+ channels were not responsible for this vasoactive effect.