Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products.
The increasing use of acrylate-based resins in dentistry has raised questions about the biocompatibility of these substances with oral tissues. The focus of the present investigation was to assess the responsiveness of blood vessels to the resin polymerization accelerating agent dimethylaminoethyl methacrylate (DMAEMA) and its degradation products dimethylethanolamine (DME) and methacrylic acid (MAA), using the rat aortic ring preparation as a tissue model. DMAEMA induced concentration-dependent relaxation of norepinephrine (NE)-contracted aortic rings with and without endothelium. N-nitro-L-arginine methyl ester (L-NAME) selectively inhibited the endothelium-dependent relaxation induced by DMAEMA, suggesting the release of nitric oxide from the endothelium by DMAEMA. Both indomethacin and glybenclamide attenuated the vasorelaxation elicited by DMAEMA in the presence as well as in the absence of endothelium, providing evidence for the role of vasorelaxant prostanoid(s) and K(ATP) channel activation in the responses observed. On the other hand, while MAA was without any apparent effect on the rat aorta, DMAEMA at high and DME at relatively low concentrations caused contraction of the tissues with and without endothelium in the absence of NE. The DME-induced contraction was inhibited by indomethacin, suggesting the involvement of contractile arachidonic acid metabolite(s) in the action of DME. This observation was supported by the findings of increased thromboxane A(2) (TXA(2)) production in aortic rings incubated with DME. Taken together, the data suggest that both DMAEMA and its degradation product, DME, are vasoactive, inducing vasorelaxation and contraction by various mechanisms that may involve the release of nitric oxide from the endothelium, the activation of smooth muscle K(ATP) channels, and the generation of vasorelaxant prostanoid(s) and TXA(2). These effects may play a role in tissue homeostasis and certain adverse conditions associated with the use of dental resin materials containing DMAEMA and/or DME.
Abebe
Worku
W
Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, CB 3710, Medical College of Georgia, Augusta, Georgia 30912-1128, USA. wabebe@mail.mcg.edu
Maddux
William F
WF
Schuster
George S
GS
Lewis
Jill B
JB
D000109:Acetylcholine / Q000494:pharmacology; D000180:Acrylic Resins / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D001672:Biocompatible Materials / Q000494:pharmacology*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003642:Deanol / Q000494:pharmacology*; D003764:Dental Materials / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects; D005905:Glyburide / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D008689:Methacrylates / Q000494:pharmacology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis; D051381:Rats; D011921:Rats, Inbred WKY; D012117:Resins, Synthetic / Q000494:pharmacology*; D013928:Thromboxane A2 / Q000096:biosynthesis; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D000180:Acrylic Resins; D001672:Biocompatible Materials; D016861:Cyclooxygenase Inhibitors; D003764:Dental Materials; D008689:Methacrylates; D011453:Prostaglandins; D012117:Resins, Synthetic; C008384:methacrylic acid; D003642:Deanol; D013928:Thromboxane A2; D000109:Acetylcholine; C049840:2-(dimethylamino)ethyl methacrylate; D005905:Glyburide; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine; D007213:Indomethacin