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Updated: Aug 16, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Effects of amifostine on glycerol-pretreated rabbit kidneys
Süreyya Barun1, Dilek Ertoy, Ergin Dileköz
1Department of Pharmacology, Medical School, Gazi University, 06510 Beşevler, Ankara, Turkey. sbarun99@hotmail.com
Abstract:
Glycerol-induced acute renal failure is an experimental model for myoglobinuric nephropathy. Amifostine is a cytoprotective agent which scavenges the free radicals. Since there is enhanced production of reactive oxygen metabolites in glycerol-induced acute renal failure, we wanted to examine whether amifostine has a protective role against vascular reactivity and histological changes in kidneys isolated from glycerol-pretreated rabbits. Perfusion pressure was recorded from kidneys obtained from rabbits injected with glycerol 3 hr before the experiments and from glycerol-pretreated and non-pretreated rabbits injected with amifostine 30 min. before the experiments. Acetylcholine-induced (10(-8)-10(-5) M) vasodilatation was tested following the construction of submaximal vasoconstriction by phenylephrine. Histological investigation was performed using light microscope. Acetylcholine-induced vasodilatation was found to be significantly decreased in glycerol, glycerol+amifostine and amifostine groups compared to controls at all concentrations. Reduction in acetylcholine-induced vasodilation was more prominent in amifostine group compared to amifostine+glycerol group. There was histological renal damage in all experimental groups and this damage was more pronounced in glycerol+amifostine group. In conclusion, contrary to expectation, amifostine per se led to histological damage and potentiated the histological damage caused by glycerol and produced a decrease in acetylcholine-induced vasodilatation. The mechanisms by which amifostine exerts its effects are not known.
Insights
Amifostine, a free radical scavenger, unexpectedly worsened kidney damage and reduced blood vessel function in a glycerol-induced acute renal failure model. Contrary to expectations, amifostine alone caused damage and potentiated glycerol
Area of Science:
- Nephrology
- Pharmacology
- Experimental Pathology
Background:
- Glycerol-induced acute renal failure serves as a model for myoglobinuric nephropathy.
- Amifostine is a cytoprotective agent known for its free radical scavenging properties.
- Increased reactive oxygen metabolites are observed in glycerol-induced acute renal failure.
Purpose of the Study:
- To investigate the potential protective role of amifostine against vascular reactivity and histological kidney damage in a glycerol-induced acute renal failure model.
- To assess the effects of amifostine on acetylcholine-induced vasodilation and renal histology in rabbits.
Main Methods:
- Kidneys were isolated from rabbits pretreated with glycerol and/or amifostine.
- Vascular reactivity was assessed by measuring acetylcholine-induced vasodilation after phenylephrine-induced vasoconstriction.
- Renal histological changes were examined using light microscopy.
Main Results:
- Acetylcholine-induced vasodilation was significantly decreased in glycerol, glycerol+amifostine, and amifostine groups compared to controls.
- The reduction in vasodilation was more pronounced in the amifostine-only group compared to the glycerol+amifostine group.
- Histological renal damage was observed in all experimental groups, being most severe in the glycerol+amifostine group.
Conclusions:
- Amifostine, contrary to expectations, caused histological renal damage on its own.
- Amifostine potentiated the renal damage induced by glycerol.
- Amifostine administration led to a decrease in acetylcholine-induced vasodilation, suggesting adverse effects on vascular function in this model.
