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

机译:黄芪总黄酮分数的影响Astragalus Chromanatus r.Shown对高血压大鼠血管紧张素II诱导的门静脉收缩。

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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.
机译:本研究的目的是进一步检查从黄芪康纳图菌的种子中提取的总黄酮(TF)的抗高血压效果的潜在机制。通过双肾单夹(2K1C)方法建立肾血管高血压大鼠(RHR)。在分离的制剂中研究了TF对门静脉收缩的影响。门静脉对血管紧张素II(Ang II)的响应表示为100mmol / L KCl诱导的最大收缩的百分比。我们将门静脉的剂量响应曲线(从10(-9)至10(-6)mmol / l)作为对照,然后观察到Tf和缬沙坦(Ang II受体阻滞剂)后曲线的变化行政。 Ang II诱导浓度依赖性增加的收缩振幅(最大增加,46.53 +/- 5.15%的100mmol / L KCl在rHR中的Ang II 10(-6)mmol / L中的收缩)。通过浓度相关的方式防止Ang II诱导的门静脉收缩(最大抑制幅度在46.53 + / -5.15%至22.525±5.15%至22.525 +/- 4.67%的100mmol / l Kcl收缩中,在10(-6)mmol / L Ang II和3.12 x 10(-1)mg / l Tf在RHR中)。 TF对Ang II诱导的门静脉收缩的影响与Valsartan相似。这些结果表明,TF的抗高血压作用归因于血管的扩张,并且与Ang II受体的阻断有关。

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