title: Attenuation of contrast material-induced renal artery vasoconstriction by nitric oxide donors.
abstract: OBJECTIVE
  The authors studied the role of the endothelium and associated endothelial pathways in contrast material-induced renal vasoconstriction.
  
  
  METHODS
  Isometric contractions in human and rabbit renal artery rings with intact and denuded endothelium were stimulated with phenylephrine and increasing concentrations of the ionic contrast material diatrizoate, the nonionic contrast materials iopamidol and iomeprol, and the dimeric contrast material iodixanol in a tissue perfusion bath. Rings with intact endothelium were incubated with endothelium-stimulating compounds such as the NO synthetase inhibitor Ng nitro-L-arginine methyl ester (L-NAME) to study the endothelium-mediated vasomotor regulation and the NO-liberating substances molsidomine (SIN-1) and nitroprusside (NPR) to study the endothelial-mediated vasorelaxation before being stimulated with contrast material.
  
  
  RESULTS
  Contrast material-induced, dose-dependent, reversible renal artery contractions are dependent on the type of contrast material. No differences in the contractions were found between intact and denuded rings. L-NAME had no effect on contrast material-induced contractions. Contractions were inhibited by the NO donors SIN-1 and NPR. SIN-1 was the most potent inhibitor.
  
  
  CONCLUSIONS
  Contrast material-induced renal vasoconstriction is endothelium-independent. Selective pharmacologic stimulation of the endothelium by NO donors, however, may still be useful in the prophylaxis of contrast material-induced renal vasoconstriction and, thus, potentially nephrotoxicity.
authors.affiliation: Department of Radiology, Medical College of Wisconsin, Milwaukee 53226, USA.
authors.forename: P
authors.initials: P
authors.lastname: Drescher
authors.forename: P O
authors.initials: PO
authors.lastname: Madsen
mesh_terms: D000818:Animals; D003287:Contrast Media / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D016232:Endothelins / Q000008:administration & dosage / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D008981:Molsidomine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D010656:Phenylephrine / Q000008:administration & dosage / Q000494:pharmacology; D011817:Rabbits; D012077:Renal Artery / Q000187:drug effects / Q000502:physiology*; D014019:Tissue Donors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D003287:Contrast Media; D016232:Endothelins; D004791:Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine; D019331:NG-Nitroarginine Methyl Ester