Renovascular smooth muscle contractility, an important factor in contrast media-induced nephrotoxicity, depends on intracellular Ca 2+ concentration, which is composed of extracellular Ca 2+ influx and intracellular Ca 2+ release. These factors were investigated in contrast media-induced renal vasoconstriction in an in vitro model.KCl-induced isometric contractions of rabbit renal artery were compared with contractions elecited y contrast media (diatrizoate, iohexol, iopamidol). Measurements were made after incubation with the Ca 2+ channel blockers nifedipine, verapamil, and diltiazem to assess the role of extracellular Ca 2+ influx and after ryanodine and thapsigargin to investigate the role of intracellular Ca 2+ release.The Ca 2+ channel blockers partially inhibited contractions induced by contrast media, while KCl-induced contractions were completely abolished., Ryanodine and thapsigargin also markedly inhibited contrast media-induced contractions.Ionic and nonionic contrast media induced quantitatively different renal vasocontractions. Ca 2+ channel blockers inhibited this vasocontraction only slightly compared with intracellular Ca 2+ release blockers.