Ginkgo biloba extract-induced relaxation of rat aorta is associated with increase in endothelial intracellular calcium level
Ginkgo biloba extract-induced relaxation of rat aorta is associated with increase in endothelial intracellular calcium level
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DOI：
10.1016/s0024-3205(01)01303-0
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发表时间：
2001-10-05
期刊：
影响因子：
6.1
通讯作者：
Kunitomo, M
中科院分区：
文献类型：
--
作者：
Kuboto, Y;Tanaka, N;Kunitomo, M
银杏叶提取物（GBE）已在法国和德国用于改善外周血管疾病的临床。在本研究中，我们研究了GBE和槲皮素的作用，以阐明GBE产生的血管扩张的药理特性。GBE中的一种成分，在Wistar大鼠胸主动脉上的作用。GBE在去甲肾上腺素预收缩的主动脉环中产生剂量依赖性松弛，而l -n - g -硝基精氨酸甲酯（L-NAME）可消除这种松弛。槲皮素产生了类似的松弛作用，L-NAME也消除了这种作用。然后，我们使用荧光共聚焦显微成像系统检查了GBE和槲皮素对培养的主动脉内皮细胞内钙水平（[Ca2+]i）的影响。GBE和槲皮素均能显著增加内皮细胞中的[Ca2+]i。槲皮素（10(-6)M）增加的[Ca2+]i通过去除细胞外Ca2+而被消除，但不受thapsigargin（钙泵抑制剂）的影响。这些发现表明，GBE产生血管舒张的主要成分是槲皮素，槲皮素可以通过增加血管内皮细胞中的[Ca2+]i来激活一氧化氮的合成和释放。(C) 2001爱思唯尔科学公司版权所有。
Ginkgo biloba extract (GBE) has been used clinically for improving peripheral vascular diseases in France and Germany. In the present study, to clarify the pharmacological properties of vasodilation produced by GBE, we examined the effect of GBE and quercetin. one of the ingredients in GBE, on the thoracic aorta isolated from Wistar rats. GBE produced a dose-dependent relaxation in the aortic ring precontracted with noradrenaline, and the relaxation was abolished by L-N-G-nitro arginine methyl ester (L-NAME). Quercetin produced a similar relaxation, which was also abolished by L-NAME. We then examined the effects of GBE and quercetin on the intracellular calcium level ([Ca2+]i) of cultured aortic endothelial cells using a fluorescent confocal microscopic imaging system. Both GBE and quercetin produced significant increases in [Ca2+]i in the endothelial cells. The increase in [Ca2+]i by quercetin (10(-6) M) was abolished by removing the extracellular Ca2+, but was not affected by thapsigargin, a calcium pump inhibitor. These findings suggest that a principal ingredient of GBE producing vasodilation is quercetin, which can activate nitric oxide synthesis and release by increasing [Ca2+]i in vascular endothelial cells. (C) 2001 Elsevier Science Inc. All rights reserved.