期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 606, 期 1-3, 页码 142-149出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2009.01.033
关键词
Ginsenoside-Rd; Hypertension (kidney); Cerebrovascular remodeling; Receptor-operated; Store-operated; Ca2+ channels
资金
- National Natural Science Foundation of China [30730105]
- National Basic Research Program of China (973Program) [2009CB521903]
- Science Foundation of Guangzhou in China
The total saponins of Panax notoginseng have been clinically used for the treatment of cardiovascular diseases and stroke in China. Our recent study has identified ginsenoside-Rd, a purified component of total saponins of P. notoginseng, as an inhibitor to remarkably inhibit voltage-in dependent Ca2+ entry. We deduced a hypothesis that the inhibition of voltage-independent Ca2+ entry might contribute to its cerebrovascular benefits, Ginsenoside-Rd was administered to two-kidney, two-clip (2k2c) stroke-prone hypertensive rats to examine its effects on blood pressure, cerebrovascular remodeling and Ca2+ entry in freshly isolated basilar arterial vascular smooth muscle cells (BAVSMCs). Its effects on endothelin-1 induced Ca2+ entry and cellular proliferation were assessed in cultured BAVSMCs. The results showed that, in vivo, ginsenoside-Rd treatment attenuated basilar hypertrophic inward remodeling in 2k2c hypertensive rats without affecting systemic blood pressure. During the development of hypertension, there were time-dependent increases in receptor-operated Ca2+ channel (ROCC)-, store-operated Ca2+ channel (SOCC)- and voltage dependent Ca2+ channel (VDCC)-mediated Ca2+ entries in freshly isolated BAVSMCs. Ginsenoside-Rd reversed the increase in SOCC- or ROCC- but not VDCC-mediated Ca2+ entry. In vitro, ginsenoside-Rd concentration-dependently inhibited endothelin-1 induced BAVSMC proliferation and Mn2+ quenching rate within the same concentration range as required for inhibition of increased SOCC- or ROCC-mediated Ca2+ entries during hypertension. These results provide in vivo evidence showing attenuation of hypertensive cerebrovascular remodeling after ginsenoside-Rd treatment. The underlying mechanism might be associated with inhibitory effects of ginsenoside-Rd on voltage-independent Ca2+ entry and BAVSMC proliferation, but not with VDCC-mediated Ca2+ entry. (C) 2009 Elsevier B.V. All rights reserved.
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