Study of cysteinyl leukotriene-1 receptor in rat renal ischemia-reperfusion injury

Renal ischemia-reperfusion (I/R) injury is a major cause of renal transplant dysfunction. Recent studies of I/R injury have focused on the function of neutrophils, the mechanisms of action of inflammatory cytokines, and oxygen free radicals, as well as other mediators. However, few reports address the cysteinyl leukotriene-1 receptor (CysLT(1)R), an important mediator of bronchial asthma in human beings. We examined the expression of CysLT(1)R in rat renal I/R injury. At laparotomy, the right kidney was harvested and the left renal artery and vein were clamped. The kidney was reperfused after 90 minutes of ischemia, and the rats were killed after 0, 3, 5, 12, or 24 hours. Expression of CysLT(1)R analyzed at immunohistochemistry was observed only in endothelial cells in nonischemic kidney. At 0 to 3 hours after reperfusion, CysLT(1)R expression on endothelial cells gradually became stronger, being most intense at 3 hours after reperfusion. Twelve hours after reperfusion, necrosis extended throughout the ischemic kidney; nearly all of the tubular epithelial cells were destroyed. At 3 to 12 hours after reperfusion, CysLT(1)R expression gradually became weaker on endothelial cells. At 24 hours after reperfusion, CysLT(1)R expression was almost at the level of that in nonischemic kidney. Expression of CysLT(1)R was noted in a rat model of renal I/R injury. Several hours after the maximal CysLT(1)R expression, we observed the maximum renal I/R injury. These results may suggest a relationship between the CysLT(1)R and renal I/R injury.