Indigo carmine enhances phenylephrine-induced contractions in an isolated rat aorta

Abstract

Background: The intravenous administration of indigo carmine has been reported to produce transiently increased blood pressure in patients. The goal of this in vitro study was to examine the effect of indigo carmine on phenylephrine-induced contractions in an isolated rat aorta and to determine the associated cellular mechanism with particular focus on the endothelium-derived vasodilators. Methods: The concentration-response curves for phenylephrine were generated in the presence or absence of indigo carmine. Phenylephrine concentration-response curves were generated for the endothelium-intact rings pretreated independently with a nitric oxide synthase inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME), a cyclooxygenase inhibitor, indomethacin, and a low-molecular-weight superoxide anion scavenger, tiron, in the presence or absence of indigo carmine. The fluorescence of oxidized dichlorofluorescein was measured in rat aortic vascular smooth muscle cells cultured in the control, indigo carmine alone and tiron plus indigo carmine. Results: Indigo carmine (10-5 M) increased the phenylephrine-induced maximum contraction in the endotheliumintact rings with or without indomethacin, whereas indigo carmine produced a slight leftward shift in the phenylephrine concentration-response curves in the endothelium-denuded rings and L-NAME-pretreated endothelium-intact rings. In the endothelium-intact rings pretreated with tiron (10-2 M), indigo carmine did not alter phenylephrine concentration-response curves significantly. Indigo carmine (10-5 M) increased the fluorescence of oxidized dichlorofluorescein in the vascular smooth muscle cells, whereas tiron abolished the indigo carmineinduced increase in oxidized dichlorofluorescein fluorescence. Conclusions: Indigo carmine increases the phenylephrine-induced contraction mainly through an endotheliumdependent mechanism involving the inactivation of nitric oxide caused by the increased production of reactive oxygen species. ? the Korean Society of Anesthesiologists, 2011.