title: Angiotensin-converting enzyme inhibitors reduce oxidative stress intensity in hyperglicemic conditions in rats independently from bradykinin receptor inhibitors.
abstract: OBJECTIVE
  To investigate whether endogenous bradykinin is involved in the antioxidant action of angiotensin-converting enzyme inhibitors (ACEIs) in acute hyperglycemia.
  
  
  METHODS
  Male Wistar rats were divided into the normoglycemic group (n=40) and the hyperglycemic group (n=40). Hyperglycemia was induced by a single intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) dissolved in 0.1 mol/L citrate buffer (pH 4.5) 72 hours before sacrifice. The normoglycemic group received the same volume of citrate buffer. Each group was divided into five subgroups (n=8): control group, captopril group, captopril + bradykinin B1 and B2 receptor antagonists group, enalapril group, and enalapril + bradykinin B1 and B2 receptor antagonists group. Captopril, enalapril, B1 and B2 receptor antagonists, or 0.15 mol/L NaCl were given at 2 and 1 hour before sacrifice. Oxidative status was determined by measuring the concentration of malondialdehyde and H2O2, and the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx).
  
  
  RESULTS
  In STZ-induced hyperglycemic rats ACEIs significantly reduced H2O2 concentration, while they significantly enhanced SOD and GPx activity. The hyperglycemic group treated simultaneously with ACEIs and bradykinin B1 and B2 receptor antagonists showed a significant decrease in H2O2 concentration compared to the control hyperglycemic group.
  
  
  CONCLUSIONS
  These results suggest the existence of the bradykinin -independent antioxidative effect of ACEIs in hyperglycemic conditions, which is not related to the bradykinin mediation and the structure of the drug molecule.
authors: Kinga Mikrut, Department of Physiology, Poznan University of Medical Sciences, Swiecickiego St., 6, 60-781 Poznan, Poland, kingaem@op.pl.
authors: Kinga
authors: K
authors: Mikrut
authors: Justyna
authors: J
authors: Kupsz
authors: Jacek
authors: J
authors: Kozlik
authors: Hanna
authors: H
authors: Krauss
authors: Ewa
authors: E
authors: Pruszynska-Oszmałek
authors: Magdalena
authors: M
authors: Gibas-Dorna
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D065168:Bradykinin Receptor Antagonists / Q000378:metabolism*; D002216:Captopril / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004656:Enalapril / Q000494:pharmacology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D006943:Hyperglycemia / Q000503:physiopathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000318:Adrenergic beta-Agonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D065168:Bradykinin Receptor Antagonists; D008315:Malondialdehyde; D004656:Enalapril; D002216:Captopril; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase