Abstract:

Aim: The imbalance between production of reactive oxygen species and antioxidant defense determines the degree of oxidative toxicity and severity of subsequent myocardial damage.We aimed to evaluate the anti-oxidative effects of neprilysin and angiotensin inhibition on cardiovascular target tissues in dexhamethasone-induced hypertensive rats. Methods: Thirty-six Wistar rats were divided into six groups. Three groups received 30 μg/kg/day dexamethasone for 14 days to induce arterial hypertension. Mean arterial blood pressure was verified by carotid artery cannulation. Ramipril (10 mg/kg), and sacubitril/valsartan (80 mg/kg) were administered for 18 days to the hypertensive and normotensive groups. Glutathione peroxidase, superoxide dismutase and malondialdehyde levels were evaluated in cardiovascular target tissues. Results: Serum and cardiac malondialdehyde levels were lower, while cardiac glutathione peroxidase and superoxide dismutase were higher in treatment groups than in control groups. Aortic malondialdehyde in sacubitril/valsartan group was lower; aortic and renal superoxide dismutase in sacubitril/valsartan and ramipril groups were significantly higher than in control group. Serum glutathione peroxidase was higher in hypertensive sacubitril/valsartan group than in hypertensive control group. Conclusion: We demonstrated that neprilysin and/or angiotensin inhibition had protective properties against oxidative stress exerted by dexhamethasone-induced hypertension in cardiovascular target organs, which may be mediated by reversal of natriuretic peptides degradation.m, hypertension, oxidative stress, dexamethasone, rat