Role of intracellular calcium stores in contrast medium—induced renal vasoconstriction
Autor: | Dieter Rauch, P. Drescher, Paul O. Madsen |
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Rok vydání: | 1996 |
Předmět: |
medicine.medical_specialty
Thapsigargin medicine.drug_class Contrast Media Calcium channel blocker Potassium Chloride chemistry.chemical_compound Renal Artery Internal medicine medicine Extracellular Animals Radiology Nuclear Medicine and imaging Channel blocker Voltage-dependent calcium channel Ryanodine Chemistry Ryanodine receptor Osmolar Concentration Smooth muscle contraction Calcium Channel Blockers Endocrinology Vasoconstriction Calcium Calcium Channels Rabbits Intracellular |
Zdroj: | Academic Radiology. 3:912-918 |
ISSN: | 1076-6332 |
DOI: | 10.1016/s1076-6332(96)80298-4 |
Popis: | Rationale and Objectives. 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. Methods. 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 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. Results. 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. Conclusion. Ionic and nonionic contrast media induced quantitatively different renal vasocontractions. Ca2+ channel blockers inhibited this vasocontraction only slightly compared with intracellular Ca2+ release blockers. |
Databáze: | OpenAIRE |
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