[Role of NO-synthase in stimulation of opiate receptors and kidney oxidative stress resistance].
It was established that dalarginum injection before ARI (acute renal insufficiency) formation prevented an increases of proteolysis, decrease of SOD (superoxide dismutase), increase of NO2-/NO3- content in kidney tissue. Antioxidant effect of opiate receptor agonist was completely abolished by preliminary injection of OR antagonist--naloxone. Aminoguanidine nitrate (inducible NO-synthase inhibitor) injection removed positive effect of OR stimulation too. Thus OR stimulation increases kidney oxidative stress resistance due to NO-synthase and SOD activation.
Orlova
E A
EA
Komarevtseva
I A
IA
D058186:Acute Kidney Injury / Q000201:enzymology / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D004195:Disease Models, Animal; D016308:Enkephalin, Leucine-2-Alanine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007668:Kidney / Q000201:enzymology / Q000378:metabolism*; D008024:Ligands; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D011957:Receptors, Opioid / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D004791:Enzyme Inhibitors; D008024:Ligands; D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D009270:Naloxone; D016308:Enkephalin, Leucine-2-Alanine; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; C040996:enkephalin-Leu, Ala(2)-Arg(6)-