ATTENUATION OF CONTRAST MATERIAL-INDUCED RENAL-ARTERY VASOCONSTRICTION BY NITRIC-OXIDE DONORS

Rationale and objectives. The authors studied the role of the endothel ium and associated endothelial pathways in contrast material-induced r enal vasoconstriction. Materials and Methods. Isometric contractions i n human and rabbit artery rings with intact and denuded endothelium we re stimulated with phenylephrine and increasing concentrations of the ionic contrast material diatrizoate, the nonionic contrast materials i opamidol 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 inhib itor N-g nitro-L-arginine methyl ester (L-NAME) to study the endotheli um-mediated vasomotor regulation and the NO-liberating substances mols idomine (SIN-1) and nitroprusside (NPR) to study the endothelial-media ted vasorelaxation before being stimulated with contrast material. Res ults. Contrast material-induced, dose-dependent, reversible renal arte ry contractions are dependent on the type of contrast material. No dif ferences in the contractions were found between intact and denuded rin gs. L-NAME had no effect on contrast-material induced contractions. Co ntractions were inhibited by the NO donors SIN-1 and NPR. SIN-1 was th e most potent inhibitor. Conclusion. Contrast material-induced renal v asoconstriction is endothelium-independent. Selective pharmacologic st imulation of the endothelium by NO donors, however, may still be usefu l in the prophylaxis of contrast material-induced renal vasoconstricti on and, thus, potentially nephrotoxicity.