1. Impact of angiotensin-converting enzyme inhibition on renal cortical nitrotyrosine content during increased extracellular glucose concentration
- Author
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Takao Saruta, Tadakazu Maeda, Naohito Ishii, Tatsuo Nagai, Yoshikazu Aoki, Nobukazu Takada, Masato Katagiri, Hideki Ikenaga, Pamela K. Carmines, and Toshio Okazaki
- Subjects
Male ,medicine.medical_specialty ,Kidney Cortex ,Renal cortex ,Clinical Biochemistry ,Angiotensin-Converting Enzyme Inhibitors ,Nitric Oxide ,Nitric oxide ,Rats, Sprague-Dawley ,Superoxide dismutase ,chemistry.chemical_compound ,Enalapril ,Superoxides ,Internal medicine ,medicine ,Animals ,Nitrates ,biology ,Superoxide Dismutase ,Superoxide ,Nitrotyrosine ,Angiotensin-converting enzyme ,General Medicine ,Rats ,Glucose ,medicine.anatomical_structure ,Endocrinology ,chemistry ,ACE inhibitor ,biology.protein ,Tyrosine ,medicine.drug - Abstract
Experiments evaluated the hypothesis that angiotensin-converting enzyme (ACE) inhibition suppresses hyperglycemia-induced nitrotyrosine (NT) production in the renal cortex.Rats were untreated (UNTR, n = 6) or received the ACE inhibitor enalapril (20 mg/kg/day; ENAL, n = 6) for 2 weeks. Renal cortical slices were incubated for 90 min in media containing 5 (normal) or 20 mmol/L (high) glucose. Superoxide anion (O2*-) and nitrate + nitrite (NO(X)) levels were measured in the media. Superoxide dismutase (SOD) activity and NT content were measured in the tissue homogenate.In the UNTR group, high glucose increased O2*- and NO(X) production by the renal cortex (P0.05 vs. normal glucose). Likewise, NT content and SOD activity of the renal cortex augmented (P0.05 vs. normal glucose). In the ENAL group, O2*- production and NT content were glucose-insensitive, but high glucose exerted an exaggerated impact on NO(X) production and SOD activity (P0.01 vs. UNTR in high glucose).Accelerated NT content in the renal cortex during high-glucose conditions was prevented by ACE inhibitor treatment. It was suggested that, apart from its anti-hypertensive effect, the mechanism of suppressed NT degradation in the renal cortex by the ACE inhibitor enhances both O2*- degradation per se and antioxidative effects including SOD activation.
- Published
- 2006
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