OBJECTIVE: Chronic inhibition of nitric oxide (NO) synthesis by Nomega-nitro-L-arginine methyl ester (L-NAME) increases vascular tissue angiotensin II activity and oxidative stress in animals by incompletely understood mechanisms. In a rat model, we investigated the role of local angiotensin II activity in the pathogenesis of increased oxidative stress. DESIGN: We studied the aortas of control rats and others receiving L-NAME or L-NAME plus an angiotensin II type 1 receptor antagonist (CS-866). RESULTS: Administration of L-NAME for 7 days significantly increased superoxide anion (O2-) and both immunoreactivity and electrophoretically demonstrable activity of redox-sensitive transcription factors (NF-kappaB and AP-1). Treatment with the angiotensin II type 1 receptor antagonist prevented all of the above changes. The observed effects of the type 1 receptor antagonist was independent of the L-NAME-induced arterial hypertension. CONCLUSIONS: These findings suggest that chronic inhibition of NO synthesis may increase vascular oxidative stress and oxidative stress-sensitive signals via the action of angiotensin II mediated via type 1 receptors.
OBJECTIVE: Chronic inhibition of nitric oxide (NO) synthesis by Nomega-nitro-L-arginine methyl ester (L-NAME) increases vascular tissue angiotensin II activity and oxidative stress in animals by incompletely understood mechanisms. In a rat model, we investigated the role of local angiotensin II activity in the pathogenesis of increased oxidative stress. DESIGN: We studied the aortas of control rats and others receiving L-NAME or L-NAME plus an angiotensin II type 1 receptor antagonist (CS-866). RESULTS: Administration of L-NAME for 7 days significantly increased superoxide anion (O2-) and both immunoreactivity and electrophoretically demonstrable activity of redox-sensitive transcription factors (NF-kappaB and AP-1). Treatment with the angiotensin II type 1 receptor antagonist prevented all of the above changes. The observed effects of the type 1 receptor antagonist was independent of the L-NAME-induced arterial hypertension. CONCLUSIONS: These findings suggest that chronic inhibition of NO synthesis may increase vascular oxidative stress and oxidative stress-sensitive signals via the action of angiotensin II mediated via type 1 receptors.
Authors: Johannes-Peter Stasch; Peter M Schmidt; Pavel I Nedvetsky; Tatiana Y Nedvetskaya; Arun Kumar H S; Sabine Meurer; Martin Deile; Ashraf Taye; Andreas Knorr; Harald Lapp; Helmut Müller; Yagmur Turgay; Christiane Rothkegel; Adrian Tersteegen; Barbara Kemp-Harper; Werner Müller-Esterl; Harald H H W Schmidt Journal: J Clin Invest Date: 2006-09 Impact factor: 14.808
Authors: Aline C D Androwiki; Lívia de Lucca Camargo; Simone Sartoretto; Gisele K Couto; Izabela M R Ribeiro; Sidney Veríssimo-Filho; Luciana V Rossoni; Lucia R Lopes Journal: Front Chem Date: 2015-03-27 Impact factor: 5.221