首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Endothelium/Nitric Oxide Mediates the Vasorelaxant and Antihypertensive Effects of the Aqueous Extract from the Stem Bark of Mammea africana Sabine (Guttiferae)
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Endothelium/Nitric Oxide Mediates the Vasorelaxant and Antihypertensive Effects of the Aqueous Extract from the Stem Bark of Mammea africana Sabine (Guttiferae)

机译:内皮/一氧化氮介导非洲象Sa(Sabine)(树皮科)茎皮水提物的血管舒张作用和降压作用

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摘要

This study evaluates the vasorelaxant and antihypertensive effects of the aqueous extract from the stem bark of M. africana (AEMA). AEMA was tested in vitro on intact or endothelium-denuded rats' aorta rings precontracted with KCl or norepinephrine in absence or in presence of L-NAME or glibenclamide. The effect of a single concentration (300 μg/mL) of AEMA was also examined on the concentration-response curve of KCl. In vivo, the antihypertensive effects of AEMA (200 mg/kg/day) were evaluated in male Wistar rats treated with L-NAME (40 mg/kg/day) for 4 weeks. AEMA relaxed aorta rings precontracted with NE or KCl with respective EC50 values of 0.36 μg/mL and 197.60 μg/mL. The destruction of endothelium or pretreatment of aorta rings with L-NAME shifted the EC50 of AEMA from 0.36 μg/mL to 40.65 μg/mL and 20.20 μg/mL, respectively. The vasorelaxant activity of M. africana was significantly inhibited in presence of glibenclamide. AEMA also significantly inhibited the concentration-response curve of KCl. Administered orally, AEMA induced acute and chronic antihypertensive effects and normalized renal NO level. These results show that the vasorelaxant activity of AEMA might be mediated by the activation of the NO-cGMP-ATP-dependent potassium channels pathway and might predominantly account for its antihypertensive effect.
机译:这项研究评估了非洲支原体(AEMA)茎皮中水提取物的血管舒张作用和降压作用。在不存在或存在L-NAME或格列本脲的情况下,在与KCl或去甲肾上腺素预收缩的完整或内皮剥除的大鼠主动脉环上进行AEMA体外测试。还检查了单一浓度(300μg/ mL)的AEMA对KCl浓度-响应曲线的影响。在体内,在接受L-NAME(40μmg/ kg /天)治疗4周的雄性Wistar大鼠中评估了AEMA(200μmg/ kg /天)的降压作用。用NE或KCl预收缩的AEMA松弛主动脉环的EC50值分别为0.36μg/ mL和197.60μg/ mL。内皮的破坏或用L-NAME预处理主动脉环使AEMA的EC50分别从0.36μg/ mL变为40.65μg/ mL和20.20μg/ mL。在格列本脲的存在下,非洲分枝杆菌的血管舒张活性被显着抑制。 AEMA还显着抑制了KCl的浓度-响应曲线。口服AEMA可以引起急性和慢性降压作用,并使肾脏NO水平正常化。这些结果表明,AEMA的血管舒张活性可能是由NO-cGMP-ATP依赖性钾离子通道的激活介导的,并且可能主要是由于其抗高血压作用。

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