선천성 고혈압 렛드에서 혈압 및 내피의 기능장해에 대한 protopanaxatriol계 배당체의 효과
Chronic hypertension is associated with impaired endothelial function such as reduced synthesis/release of endothelium-derived relaxing factor(EDRF, nitric oxide) and increased synthesis/release of endothelium-derived contracting factor(EDCF) including prostaglandin endoperoxide($PGH_2$) , superoxid...
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Veröffentlicht in: | 고려인삼학회지 1997, Vol.21 (2), p.119-124 |
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Format: | Artikel |
Sprache: | kor |
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Zusammenfassung: | Chronic hypertension is associated with impaired endothelial function such as reduced synthesis/release of endothelium-derived relaxing factor(EDRF, nitric oxide) and increased synthesis/release of endothelium-derived contracting factor(EDCF) including prostaglandin endoperoxide($PGH_2$) , superoxide anion both in animals and in humans. We have previously shown that ginsenosides lower the blood pressure and enhance the release of nitric oxide(NO) from endothelial cells in the rat aorta of the normotensive rats. The aim of the present study is to examine whether in vivo treatment of spontaneously hypertensive rats(SHRs) with protopanaxatriol ginsenosides(PPT) reduces the blood pressure and improves endothelial function in the isolated thoracic aorta of SHR. In addition, the contractile response to $PGH_2$ and superoxide anion in the aorta treated with PPT was assessed. SHRs at the age of 16 weeks were savaged with PPT(30 mg/kg/ day) for 2 weeks and systolic blood pressure was measured by the tail-cuff method. Whereas blood pressure was significantly increased in SHRs by 5.4 mmHg during this period of treatment, treatment of SHRs with PPT blocked the elevation of blood pressure. Endothelium-dependent relaxation to acetylcholine was significantly increased in the PPT-treated animals. $PGH_2$- and oxygen-derived free radical-induced contractions were significantly suppressed in aortic rings without endothelium from PPT-treated SHR. These findings indicate that PPT reduces the blood pressure of SHR, which may be associated with either increase of NO release or by antagonizing superoxide anion and PGH2 in the aortic smooth muscle. |
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ISSN: | 1016-2615 |