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논문 기본 정보

자료유형
학술저널
저자정보
Lim, Dong-Yoon (Department of Pharmacology, College of Medicine, Chosun University) Lee, Eun-Sook (Department of Pharmacology, College of Medicine, Chosun University) Park, Hyeon-Gyoon (Department of Pharmacology, College of Medicine, Chosun University) Kim, Byeong-Cheol (Department of Pharmacology, College of Medicine, Chosun University) Hong, Soon-Pyo (Department of Internal Medicine [Cardiology], College of Medicine, Chosun University) Lee, Eun-Bang (Natural Products Research Institute, Seoul National University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제26권 제3호
발행연도
2003.1
수록면
214 - 223 (10page)

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The present study was conducted to investigate the effects of green tea extract (GTE) on arterial blood pressure and contractile responses of isolated aortic strips of the normotensive rats and to establish the mechanism of action. The phenylephrine ($10^{-6}~10^{-5}M$)-induced contractile responses were greatly inhibited in the presence of GTE (0.3~1.2 mg/mL) in a dose-dependent fashion. Also, high potassium ($3.5{\times}10^{-2}~5.6{\times}10^{-2}{\;}M$)-induced contractile responses were depressed in the presence of 0.6~1.2 mg/mL of GTE, but not affected in low concentration of GTE (0.3 mg/mL). However, epigallocatechin gallate (EGCG, $4~12{\;}{\mu}g/mL$) did not affect the contractile responses evoked by phenylephrine and high $K^+$. GTE (5~20 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 $\alpha_1$-receptors. GTE also causes the relaxation in the isolated aortic strips of the rat via the blockade of adrenergic $\alpha_1$-receptors, in addition to the unknown direct mechanism. It seems that there is a big difference in the vascular effect between GTE and EGCG.

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