Modulation of Hemodynamics, Endogenous Antioxidant Enzymes, and Pathophysiological Changes by Angiotensin-Converting Enzyme Inhibitors in Pressure-Overload Rats

Introduction: We sought to assess the role of angiotensin-converting enzyme (ACE) inhibitors on systolic blood pressure (BP), endogenous antioxidant enzymes and histopathological changes in pressure-overload rats. Methods: Pressure overload was produced in male rats by abdominal aortic banding (AAB) using a blunt 22-gauge needle, as a model of cardiac hypertrophy. After surgery, AAB-induced hypertensive (AABIH) groups were treated with captopril 4 mg and ramipril 10 mg/kg per day p.o. for 16 weeks. At 16 weeks, rats were observed for general characteristics and mortality, non-invasive blood pressure (NIBP) and endogenous antioxidant enzyme catalase and superoxide dismutase (SOD) activity and histological evaluation of target organs. Results: In the AABIH group a significant increase in systolic BP was observed in week 3 (149.3 +/- 0.821) and persisted until week 16, along with lower levels of serum catalase (144.7 +/- 2.204) and SOD (12.92 +/- 0.4601) activity compared to the control group. Captopril and ramipril treated groups showed a significantly smaller increase in systolic BP (25.47 +/- 3.685, 20.21 +/- 3.306) and greater serum SOD (27.33 +/- 2.338, 28.95 +/- 1.143) and catalase (181.7 +/- 8.407, 187.9 +/- 8.497) activity, respectively, than the hypertensive rats. The histological changes induced in target organs (heart, liver, kidneys and thoracic aorta) in AABIH rats were attenuated in treated rats. Conclusion: ACE-inhibition causes an improvement in myocardial antioxidant reserve, reduces oxidative stress, and prevents pathophysiological alterations, while showing a trend for potential target organ protection in hypertensive rats.