2-Chloroethanol (2-CE) is a commonly used solvent in industry; unfortunately, severe hypotension is one of main toxic signs during intoxication. Calcium ion modulation is considered to be an important role of vasorelaxation. The aim of this study is to evaluate either 2-CE or its main metabolite, chloroacetaldehyde (CAA), possible cause of hypotension, by using isolated rat aortic rings. Results revealed that 2-CE caused a weakly relaxation in the phenylephrine (PE) pre-induced endothelium-intact aortic rings. However, its metabolite, CAA induced vasorelaxation and showed dose dependency in endothelium-intact and -denuded aortic rings. The half inhibitory concentration (IC50) of 2-CE exceeded 50mM; meanwhile, the IC50 values of CAA in the endothelium-intact and -denuded aortic rings were 3.3 and 2.7mM, respectively. The CAA-induced relaxation could be significantly attenuated by adding calcium (CaCl2) and various Ca2+ channel blockers, dantrolene, nifedipine, and NiCl2. Nifedipine presents the most strong inhibition effect among the calcium blockers. In conclusion, it is suggested that the hypotension effect of 2-CE intoxicated cases may be mainly mediated by its metabolite CAA, and calcium channels are partially involved inducing the vasorelaxation.
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