Lipid peroxidation and renal injury in renal ischemic reperfusion: effect ofangiotensin inhibition.
OBJECTIVE
To investigate the role of angiotensin inhibition on lipid peroxidation (LPO) and renal pathology in ischemic reperfusion (IR).


METHODS
Male Wistar rats were subjected to 15-, 30-, 45- or 60- minutes ofrenal ischemia (I) by left renal artery occlusion. In the 30-minute I group, reperfusion (R) for I day (13,R) was performed in additional animals that had been treated with water, angiotensin converting enzyme inhibitor (ACE]; enalapril 5 mg/kg/d), or angiotensin receptor type 1 blocker (ARB; losartan 10 mg/kg/d) one day before I and were continued for 1 day after R. Renal tissue malondialdehyde (MDA), an indicator of LPO, was examined during I and IR periods. Renal pathology was also determined.


RESULTS
During ischemia, renal tissue MDA levels were increased throughout the 60-minute ischemic period and was maximum at 30 minutes of ischemia (p < 0.01). Histological changes in 30-minutes I group showed slight tubular cell congestion and mild interstitial edema. One day after reperfusion, MDA levels were still elevated (p < 0. 01) when compared with sham. Progression of renal pathology was observed after I day of reperfusion. Both ACEI and ARB could attenuate the heightened MDA levels (p < 0.01). IR-induced renal injury was markedly diminished by administration ofACEI as well as by ARB.


CONCLUSIONS
These results indicate that inhibition of angiotensin could reduce lipid peroxidation and ameliorate renal injury during IR condition.
Seujang
Yuyen
Y
Department of Physiology, Faculty of Medicine, Chulalongkorn University Bangkok 10330, Thailand.
Kittikowit
Wipawee
W
Eiam-Ong
Somchai
S
Eiam-Ong
Somchit
S
D000803:Angiotensin I / Q000037:antagonists & inhibitors*; D000818:Animals; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*
D000803:Angiotensin I