Why the study?
Do ACE inhibitors reduce oxidative stress in acute hyperglycemia independently of bradykinin receptors in rats?
Do ACE inhibitors reduce oxidative stress in acute hyperglycemia independently of bradykinin receptors in rats?
ACE inhibitors exert an antioxidant effect in acute hyperglycemia that is independent of bradykinin mediation.
ACEIs may exert bradykinin-independent antioxidant effects in rat hyperglycemia; hypothesis-generating and leaves human translation open.
AIM: 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. CONCLUSION: 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.
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Mikrut et al. (2016) studied this question.
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