Prevention of Hypertension, Cardiovascular Damage and Endothelial Dysfunction with Green Tea Extracts

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• 作者：Michele Antonello ; Domenico Montemurro ; Massimo Bolognesi ; Marco Di Pascoli ; Anna Piva ; Franco Grego ; Daniele Sticchi ; Luisa Giuliani ; Spiridione Garbisa ; Gian Paolo Rossi
• 关键词：Green tea ; endothelium ; hypertension ; angiotensin II
• 刊名：American Journal of Hypertension
• 出版年：2007
• 出版时间：December 2007
• 年：2007
• 卷：20
• 期：12
• 页码：1321-1328
• 全文大小：367 K

文摘

Background

We investigated the effect of green tea extract (GTE) in arterial hypertension with high oxidative stress. Angiotensin (Ang) II induces endothelial dysfunction (ED) that is crucial for the development of atherosclerosis and hypertension.

Methods

Male Sprague-Dawley rats, 13 weeks old, randomly assigned to drinking water with or without GTE (6 mg/mL) received a vehicle, a high (700 μg/kg/d) or a low (350 μg/kg/d) Ang II dose for 13 days, by osmotic mini-pumps. Blood pressure (BP) was measured with telemetry. After sacrifice, left ventricular (LV) mass index, small mesenteric artery media-to-lumen ratio, and concentration–response curves of phenylephrine-precontracted arteries to acetylcholine were evaluated. The effect of the superoxide dismutase (SOD-1) analog tempol on artery responses to acetylcholine was assessed. Oxidative stress was measured by plasma hydroperoxides and nitrotyrosine levels. The mRNA of heme oxygenase 1 (HO-1), NADPH oxidase endothelial p22^phox subunit, and SOD-1 was also measured in the aorta.

Results

Compared with vehicle high Ang II increased BP, LV mass index, media-to-lumen ratio, and hydroperoxide radicals. The GTE blunted these increases, prevented the increase in HO-1, p22^phox, and SOD-1 mRNA in aorta caused by Ang II, and reduced them below baseline levels. Low Ang II dose increased BP values and plasma hydroperoxides only during the first week. Both Ang II doses shifted rightward the curves to acetylcholine; this was prevented in vivo by GTE and abolished in vitro by tempol.

Conclusions

The GTE prevented hypertension and target organ damage induced by a high Ang II dose, likely by prevention or scavenging of superoxide anion generation.