CAPTOPRIL PREVENTS THE OXIDATIVE DAMAGE TO PROTEINS AFTER RENAL ISCHEMIA-REPERFUSION INJURY - ROLE OF ENDOTHELIN-1

Ischemia reperfusion (I/R) injury is one of the leading causes of the transplanted organ loss. In this experimental study, we investigated t he effect of captopril on endothelin and eicosanoid release in I/R inj ury of the kidney. Rats were subjected to 60 min ischemia and 60 min o f reperfusion of the left kidney in control and captopril groups. Tiss ue protein oxidation products, PGE(2) and LTB(4) levels and plasma end othelin-l (ET-I) like activity were determined in sham operated, contr ol and captopril groups. There were no differences in the LTB, levels among the groups. ET-1 and PGE(2), levels and protein oxidation produc ts increased in the control group when compared with the sham. Captopr il further increased both PGE(2) and ET-l concentrations and prevented protein oxidation. The increased Ei-l concentrations in the captopril treated group may imply the protective role of endothelin as the sign ificant increase in protein oxidation products was reversed by captopr il infusion. This has led us to believe that captopril might be useful in preventing I/R injury of the kidney. Also the release of endotheli n from the vascular endothelium is increased by captopril and may be m ediated by PGE(2).