Role of intracellular calcium stores in contrast medium-induced renal vasoconstriction.

Abstract

Renovascular smooth muscle contractility, an important factor in contrast media-induced nephrotoxicity, depends on intracellular Ca2+ concentration, which is composed of extracellular Ca2+ influx and intracellular Ca2+ 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 elicited by contrast media (diatrizoate, iohexol, iopamidol). Measurements were made after incubation with the Ca2+ channel blockers nifedipine, verapamil, and diltiazem to assess the role of extracellular Ca2+ influx and after ryanodine and thapsigargin to investigate the role of intracellular Ca2+ release. The Ca2+ 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. Ca2+ channel blockers inhibited this vasocontraction only slightly compared with intracellular Ca2+ release blockers.