EDRF-RELEASE AND CA++-CHANNEL BLOCKADE BY MAGNOLOL, AN ANTIPLATELET AGENT ISOLATED FROM CHINESE HERB MAGNOLIA-OFFICINALIS, IN RAT THORACIC AORTA

被引：117

作者：

TENG, CM ^{[1
]}

YU, SM ^{[1
]}

CHEN, CC ^{[1
]}

HUANG, YL ^{[1
]}

HUANG, TF ^{[1
]}

机构：

[1] NATL RES INST CHINESE MED,TAIPEI,TAIWAN

来源：

LIFE SCIENCES | 1990年 / 47卷 / 13期

关键词：

D O I：

10.1016/0024-3205(90)90176-R

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Magnolol is an antiplatelet agent isolated from Chinese herb Magnolia officinalis. It inhibited norepinephrine (NE, 3 μM)-induced phasic and tonic contractions in rat thoracic aorta. At the plateau of the NE-induced tonic contraction, addition of magnolol caused two phases (fast and slow) of relaxation. These two relaxations were concentration-dependent (10-100 μg/m1), and were not inhibited by indomethacin (20 μM). The fast relaxation was completely antagonized by hemoglobin (10 μM) and methylene blue (50 μM), and disappeared in de-endothelialized aorta while the slow relaxation was not affected by the above treatments. Magnolol also inhibited high potassium (60 mM)-induced, calcium-dependent (0.03 to 3 mM) contraction of rat aorta in a concentration-dependent manner. 45Ca++ influx induced by high potassium or NE was markedly inhibited by magnolol. Cyclic GMP, but not PGI2, was increased by magnolol in intact, but not in de-endothelialized aorta. It is concluded that magnolol relaxed vascular smooth muscle by releasing endothelium-derived relaxing factor (EDRF) and by inhibiting calcium influx through voltage-gated calcium channels. © 1990.

引用

页码：1153 / 1161

页数：9

共 22 条

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