Drescher P, Rauch D, Madsen P O
Department of Radiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Acad Radiol. 1996 Nov;3(11):912-8. doi: 10.1016/s1076-6332(96)80298-4.
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.
肾血管平滑肌收缩性是造影剂诱导的肾毒性的一个重要因素，它取决于细胞内Ca2+浓度，而细胞内Ca2+浓度由细胞外Ca2+内流和细胞内Ca2+释放组成。在体外模型中研究了这些因素在造影剂诱导的肾血管收缩中的作用。
将氯化钾诱导的兔肾动脉等长收缩与造影剂（泛影葡胺、碘海醇、碘帕醇）诱导的收缩进行比较。在用钙通道阻滞剂硝苯地平、维拉帕米和地尔硫䓬孵育后进行测量，以评估细胞外Ca2+内流的作用，在用ryanodine和毒胡萝卜素孵育后进行测量，以研究细胞内Ca2+释放的作用。
钙通道阻滞剂部分抑制了造影剂诱导的收缩，而氯化钾诱导的收缩则完全被消除。Ryanodine和毒胡萝卜素也显著抑制了造影剂诱导的收缩。
离子型和非离子型造影剂诱导的肾血管收缩在数量上有所不同。与细胞内Ca2+释放阻滞剂相比，钙通道阻滞剂对这种血管收缩的抑制作用较小。
