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Updated: Jun 5, 2026
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Homocysteine-dependent endothelial dysfunction induced by renal ischemia/reperfusion injury
Yagnik S Bhalodia1, Navin R Sheth, Jitendra D Vaghasiya
1Department of Pharmaceutical Sciences, Jodhpur National University, Narnadi, Jodhpur, Rajasthan, India. yagnikbhalodia@gmail.com
Background:
Elevation of serum homocysteine is considered to contribute to endothelial dysfunction, which is considered to be the initial event in vascular disease following renal transplantation. We sought to investigate whether an association existed between serum homocysteine levels and endothelial dysfunction after renal ischemia/reperfusion (I/R) injury.
Materials And Methods:
Acetylcholine (Ach)-induced endothelium-dependent and sodium nitroprusside (SNP)-induced endothelial-independent relaxation responses were determined in thoracic aortas from different I/R groups. A correlation analysis was performed between Ach responses and homocysteine levels.
Results:
Long-term I/R injury decreased the responses to acetylcholine and the pD2 values of the concentration response curves compared with controls. While vascular responses to SNP were unchanged among all groups. Homocysteine levels correlated with the pD2 values of acetylcholine among control and I/R groups, indicating that the increase in homocysteine was associated with decreased sensitivity to acetylcholine. In short-term I/R rats, no association was observed between these parameters.
Conclusion:
These data suggest a possible link between serum homocysteine and decreased vascular reactivity to endothelium-dependent relaxation in I/R aorta.
