The vasodilatory effect of a synthetic polymer‐based root canal material on thoracic aorta

Abstract

To test the hypothesis that, Epiphany, either in its mixed form or as separate components, can alter the vascular reactivity of isolated rat thoracic aorta. The possible mechanism of its vascular action was also investigated. The relaxant effect of the base, the catalyst and mixed Epiphany on isolated rat aortic rings pre-contracted with phenylephrine (PE) was tested. The aortic rings were then incubated with either nitric oxide synthase (NOS) inhibitor, cyclooxygenase (COX) inhibitor or K(+) channel inhibitors; after pre-contraction with PE, relaxations to the various compounds of Epiphany were examined. In another set of experiments, to investigate the Ca(2+)channel antagonistic effect of the Epiphany, the effect of these compounds in Ca(2+)-free solution on extracellular Ca(2+)(CaCl(2))-induced contraction in high-K(+) pre-challenged rings (in K(+)-depolarized rings) was examined to determine whether the direct inhibition of [Ca(2+)] influx increase accounted for the vasodilatory effects of these compounds. For comparison, L-type Ca(2+)channel blocker nifedipine (1 micromol L(-1)), instead of Epiphany compounds, was assayed in adjacent rat aortic rings in parallel. The catalyst and the mixture of Epiphany induced concentration-dependent relaxations. However, the base of Epiphany did not cause relaxation in rat aorta. The relaxation responses were not significantly altered by incubation of aorta with NOS, COX and potassium channel inhibitors. Whilst nifedipine, the catalyst and the mixture of Epiphany inhibited CaCl(2)-induced contractions (P < 0.05), the base of Epiphany did not inhibit CaCl(2)-induced contractions significantly (P > 0.05). Epiphany induced relaxation of rat aorta via a calcium antagonistic effect. Provided that the vasodilatory effect elicited by Epiphany can be reversed by the circulation, its haemorrhagic potential by virtue of permanent vascular dilatation can be ignored.