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沙苑子总黄酮部位对高血压大鼠血管紧张素II诱导的门静脉收缩的影响

Effect of total flavonoid fraction of Astragalus complanatus R. Brown on angiotensin II-induced portal-vein contraction in hypertensive rats.

作者信息

Xue B, Li Jx, Chai Q, Liu Zx, Chen Lb

机构信息

Department of Pathophysiology, School of Medicine, Shandong University, Jinan 250012, PR China.

出版信息

Phytomedicine. 2008 Sep;15(9):759-62. doi: 10.1016/j.phymed.2007.11.030. Epub 2008 Apr 11.

Abstract

The objective of the present study was to examine further the underlying mechanism of the antihypertensive effect of the total flavonoid (TF), extracted from the seed of Astragalus complanatus R.Brown. Renovascular hypertension rats (RHR) were established by the two-kidney one clip (2K1C) method. The effect of TF on the contraction of portal vein was studied in an isolated preparation. The response of portal vein to angiotensin II (Ang II) was expressed as a percentage of the 100 mmol/l KCl induced maximum contraction. We took the dose-response curve of portal vein to Ang II (from 10(-9) to 10(-6) mmol/l) as the control and then observed the change of curve after TF and Valsartan (Ang II receptor blocker) administration. Ang II induced a concentration-dependent increase of the contraction amplitude (maximal increase, 46.53+/-5.15% of 100 mmol/l KCl induced contraction at Ang II 10(-6) mmol/l in RHR). The Ang II-induced portal vein contraction was prevented by TF with a concentration related manner (maximal inhibition amplitude from 46.53+/-5.15% to 22.525+/-4.67% of 100 mmol/l KCl contraction at 10(-6)mmol/l Ang II and 3.12 x 10(-1) mg/l TF in RHR). The effect of TF on Ang II-induced portal vein contraction was similar to Valsartan. These results showed that the antihypertensive action of TF was attributed to the dilation of vessels and is related to the blockade of the Ang II receptor.

摘要

本研究的目的是进一步探讨从扁茎黄芪种子中提取的总黄酮(TF)的降压作用机制。采用两肾一夹(2K1C)法制备肾血管性高血压大鼠(RHR)。在离体标本上研究TF对门静脉收缩的影响。门静脉对血管紧张素II(Ang II)的反应以100 mmol/l氯化钾诱导的最大收缩的百分比表示。以门静脉对Ang II(浓度范围为10^(-9)至10^(-6) mmol/l)的剂量反应曲线作为对照,然后观察给予TF和缬沙坦(Ang II受体阻滞剂)后曲线的变化。Ang II诱导收缩幅度呈浓度依赖性增加(在RHR中,当Ang II浓度为10^(-6) mmol/l时,最大增加幅度为100 mmol/l氯化钾诱导收缩的46.53±5.15%)。TF以浓度相关的方式抑制Ang II诱导的门静脉收缩(在RHR中,当Ang II浓度为10^(-6) mmol/l且TF浓度为3.12×10^(-1) mg/l时,最大抑制幅度从100 mmol/l氯化钾收缩的46.53±5.15%降至22.525±4.67%)。TF对Ang II诱导的门静脉收缩的作用与缬沙坦相似。这些结果表明,TF的降压作用归因于血管舒张,且与阻断Ang II受体有关。

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