Lim Dong-Yoon, Lee Eun-Sook, Park Hyeon-Gyoon, Kim Byeong-Cheol, Hong Soon-Pyo, Lee Eun-Bang
Department of Pharmacology, College of Medicine, Chosun University, Gwangju 501-759, Korea.
Arch Pharm Res. 2003 Mar;26(3):214-23. doi: 10.1007/BF02976833.
The present study was conducted to investigate the effects of green tea extract (GTE) on arteral blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine (10(-8) approximately 10(-5) M)-induced contractile responses were greatly inhibited in the presence of GTE (0.3 approximately 1.2 mg/mL) in a dose-dependent fashion. Also, high potassium (3.5 x 10(-2) approximately 5.6 x 10(-2) M)-induced contractile responses were depressed in the presence of 0.6 approximately 1.2 mg/mL of GTE, but not affected in low concentration of GTE (0.3 mg/mL). However, epigallocatechin gallate (EGCG, 4 approximately 12 microg/mL) did not affect the contractile responses evoked by phenylephrine and high K+. GTE (5 approximately 20 mg/kg) given into a femoral vein of the normotensive rat produced a dose-dependent depressor response, which is transient. Interestingly, the infusion of a moderate dose of GTE (10 mg/kg/30 min) made a significant reduction in pressor responses induced by intravenous norepinephrine. However, EGCG (1 mg/kg/30 min) did not affect them. Collectively, these results obtained from the present study demonstrate that intravenous GTE causes a dose-dependent depressor action in the anesthetized rat at least partly through the blockade of adrenergic alpha1-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic alpha1-receptors, in addition to the unknown direct mechanism. It seems that there is a big difference in the vascular effect between GTE and EGCG.
本研究旨在探讨绿茶提取物（GTE）对正常血压大鼠动脉血压及离体主动脉条收缩反应的影响，并确定其作用机制。在存在GTE（0.3～1.2mg/mL）时，去氧肾上腺素（10⁻⁸～10⁻⁵M）诱导的收缩反应以剂量依赖性方式受到显著抑制。此外，在存在0.6～1.2mg/mL GTE时，高钾（3.5×10⁻²～5.6×10⁻²M）诱导的收缩反应受到抑制，但在低浓度GTE（0.3mg/mL）时不受影响。然而，表没食子儿茶素没食子酸酯（EGCG，4～12μg/mL）对去氧肾上腺素和高钾诱导的收缩反应没有影响。将GTE（5～20mg/kg）注入正常血压大鼠的股静脉会产生剂量依赖性的降压反应，且该反应是短暂的。有趣的是，输注中等剂量的GTE（10mg/kg/30min）可使静脉注射去甲肾上腺素诱导的升压反应显著降低。然而，EGCG（1mg/kg/30min）对其没有影响。总体而言，本研究获得的这些结果表明，静脉注射GTE至少部分通过阻断肾上腺素能α1受体在麻醉大鼠中引起剂量依赖性的降压作用。除了未知的直接机制外，GTE还通过阻断肾上腺素能α1受体使大鼠离体主动脉条松弛。似乎GTE和EGCG在血管效应上存在很大差异。
