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(Hypertension. 2005;45:1188.)
© 2005 American Heart Association, Inc.
Original Articles |
From the Department of Geriatric Medicine (M.A., K.N., H.X., W.Y., N.S., K.K., K.T.), Kyorin University School of Medicine, Tokyo, Japan; Department of Geriatric Medicine (T.W.), Graduate School of Medicine, University of Tokyo, Japan; Department of Biochemistry (M.O.-I., S.N.), Kyorin University School of Medicine, Tokyo, Japan; Department of Medical Biochemistry (M.H.), Ehime University School of Medicine, Japan.
Correspondence to Masahiro Akishita, MD, PhD, Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail akishita-tky{at}umin.ac.jp
The role of the renin-angiotensin system in oxidative stressinduced apoptosis of endothelial cells (ECs) was investigated using a rat model and cultured ECs. EC apoptosis was induced by 5-minute intra-arterial treatment of a rat carotid artery with 0.01 mmol/L H2O2 and was evaluated at 24 hours by chromatin staining of en face specimens with Hoechst 33342. Although activity of angiotensin-converting enzyme in arterial homogenates was not increased, administration of an angiotensin-converting enzyme inhibitor temocapril for 3 days before H2O2 treatment inhibited EC apoptosis, followed by reduced neointimal formation 2 weeks later. Also, an angiotensin II type 1 (AT1) receptor blocker (olmesartan) inhibited EC apoptosis, whereas angiotensin II administration accelerated apoptosis independently of blood pressure. Next, cultured ECs derived from a bovine carotid artery were treated with H2O2 to induce apoptosis, as evaluated by DNA fragmentation. Combination of angiotensin II and H2O2 dose-dependently increased EC apoptosis and 8-isoprostane formation, a marker of oxidative stress. Conversely, temocapril and olmesartan reduced apoptosis and 8-isoprostane formation induced by H2O2, suggesting that endogenous angiotensin II interacts with H2O2 to elevate oxidative stress levels and EC apoptosis. Neither an AT2 receptor blocker, PD123319
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Key Words: angiotensin apoptosis carotid arteries endothelium free radicals
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