endothelin-1 and iopromide

Iodinated contrast media (CM) can induce apoptosis and necrosis of renal tubular cells. The injuries of endothelial cells induced by CM on the systemic condition have not been fully understood. To assess the toxic effects of non-ionic CM on the glomerular and aortic endothelial cells, iopromide and iodixanol, two kinds of representative non-ionic CM, were used for the in vivo study. Sixty aged rats were respectively received the agents or normal sodium intravascularly. No obvious apoptosis and morphological change was detected in the glomerular and aortic endothelial cells apart from renal tubules after CM administration. However, expressions of the nitric oxide synthase (eNOS) in glomerular endothelium were decreased at 12h after CM injection. Furthermore, plasma creatinine and endothelin-1 were increased and plasma nitric oxide (NO) was decreased significantly after CM administration. However, we failed to observe the significant increase of plasma von Willebrand Factor. These results suggest that non-ionic iodinated CM do not induce apoptosis and necrosis of glomerular and aortic endothelial cells in vivo. Decreased eNOS expression and increased plasma endothelin-1 may be involved in non-ionic iodinated CM-induced endothelial dysfunction and kidney injury.

Topics: Age Factors; Animals; Aorta, Abdominal; Apoptosis; Contrast Media; Creatinine; Endothelin-1; Endothelium, Vascular; Iohexol; Kidney Cortex; Kidney Glomerulus; Male; Microscopy, Electron, Transmission; Nitric Oxide; Nitric Oxide Synthase Type III; Rats; Rats, Wistar; Toxicity Tests; Triiodobenzoic Acids

High osmolal ionic radiocontrast media (RCM) cause vascular release of endothelin-1 (ET-1) and activate mast cells. Iomeprol, a nonionic RCM, has recently been reported not to activate cardiac mast cells. This coronary angiography study was performed to extend those findings using another nonionic RCM, iopromide, and to further determine whether iopromide causes release of ET-1.. Pulmonary artery plasma ET-1, histamine and serum tryptase were determined before and 30 min following angiography with iopromide in 11 subjects. ET-1, histamine and tryptase were measured using immunoassays.. The concentrations of ET-1 (1.36 +/- 0.66 pg/ml), histamine (2.63 +/- 1.15 nM), and beta (<1 microg/l) as well as total tryptase (8.25 +/- 4.63 microg/l) in the preangiography samples were within the normal range. Following angiography, the concentrations of ET-1 (0.95 +/- 0.80 pg/ml), histamine (3.08 +/- 1.06 nM), and beta (<1 microg/l) and total tryptase (7.00 +/- 5.56 microg/l) were not significantly different. None of the subjects demonstrated a postangiography increase in mediator concentration.. This study demonstrates the lack of release of ET-1 by iopromide. The lack of cardiac mast cell activation by iopromide is consistent with the report that iomeprol also does not activate cardiac mast cells.

Topics: Adult; Aged; Cardiac Catheterization; Contrast Media; Coronary Angiography; Endothelin-1; Histamine Release; Humans; Iohexol; Male; Mast Cells; Middle Aged; Prospective Studies; Radiopharmaceuticals; Serine Endopeptidases; Tryptases