Comparative effects of L-arginine and vitamin C pretreatment in SHR with induced postischemic acute renal failure.
Postischemic acute renal failure is worsened when occurs in a various conditions with impaired nitric oxide (NO) synthesis, such as arterial hypertension. Reoxygenation itself increases ischemic injury through the massive production of oxygen-free radicals. Therefore, we have directed our investigations to effects of both NO donor and antioxidant treatment on course of acute renal failure in experimental hypertension. Experiments were performed in anesthetized, adult male spontaneously hypertensive rats. In ARF groups the right kidney was removed, and rats were subjected to renal ischemia by clamping the left renal artery for 40 min. Experimental group received NO donor L-arginine (2 g/kg b.m.) (LArg group), or oxidant scavenger vitamin C (100 mg/kg b.m.) (Vit C group) during 3 days before the period of ischaemia. All parameters were measured 24 h after reperfusion. The mean arterial pressure was markedly reduced and renal vascular resistance significantly dropped in the ARF+L-Arg group vs. ARF group. Tubular injuries were similar between the ARF+L-Arg and ARF groups. Intensity of tubular necrosis and dilatation was markedly reduced in ARF+Vit C group in comparison to ARF. L-arginine failed to reduce tubular injury, despite its evident improvement of systemic and renal haemodynamic, thus NO seems to act as a double-egged sword, but reduction of tubular injury promotes vitamin C as an effective chemoprotectant against ishemia-reperfusion tubular injury in hypertension.
Miloradović
Zoran
Z
Institute for Medical Research, University of Belgrade, Dr. Subotića 4, 11129 Belgrade, P.O.Box 102, Serbia. zokim@imi.bg.ac.yu
Mihailović-Stanojević
Nevena
N
Grujić-Milanović
Jelica
J
Ivanov
Milan
M
Kuburović
Gordana
G
Marković-Lipkovski
Jasmina
J
Jovović
Durdica
D
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001120:Arginine / Q000494:pharmacology* / Q000627:therapeutic use; D001205:Ascorbic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000150:complications*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D051437:Renal Insufficiency / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
D000975:Antioxidants; D009569:Nitric Oxide; D001120:Arginine; D001205:Ascorbic Acid