title: 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, N(ω)-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 endothelium-intact 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 carmine-induced increase in oxidized dichlorofluorescein fluorescence.
  
  
  CONCLUSIONS
  Indigo carmine increases the phenylephrine-induced contraction mainly through an endothelium-dependent mechanism involving the inactivation of nitric oxide caused by the increased production of reactive oxygen species.
authors.affiliation: Department of Anesthesiology and Pain Medicine, Jeju National University School of Medicine, Jeju, Korea.
authors.forename: Yun Suk
authors.initials: YS
authors.lastname: Choi
authors.forename: Seong-Ho
authors.initials: SH
authors.lastname: Ok
authors.forename: Seung Min
authors.initials: SM
authors.lastname: Lee
authors.forename: Sang-Seung
authors.initials: SS
authors.lastname: Park
authors.forename: Yu Mi
authors.initials: YM
authors.lastname: Ha
authors.forename: Ki Churl
authors.initials: KC
authors.lastname: Chang
authors.forename: Hye Jung
authors.initials: HJ
authors.lastname: Kim
authors.forename: Il-Woo
authors.initials: IW
authors.lastname: Shin
authors.forename: Ju-Tae
authors.initials: JT
authors.lastname: Sohn