Laboratory of Animal Physiology and Phytopharmacology, Department of Animal Biology, University of Dschang, P.O. Box 67, Dschang, Cameroon.
Evid Based Complement Alternat Med. 2012;2012:961741. doi: 10.1155/2012/961741. Epub 2012 Sep 12.
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.
本研究评估了非洲吊灯树茎皮水提物（AEMA）的血管舒张和降压作用。在体外，AEMA 被测试在完整或去内皮的大鼠主动脉环上，这些主动脉环预先用 KCl 或去甲肾上腺素收缩，而不存在或存在 L-NAME 或格列本脲的情况下。还检查了 AEMA 的单一浓度（300μg/mL）对 KCl 浓度反应曲线的影响。在体内，在接受 L-NAME（40mg/kg/天）治疗 4 周的雄性 Wistar 大鼠中评估了 AEMA（200mg/kg/天）的降压作用。AEMA 松弛了用 NE 或 KCl 预收缩的主动脉环，EC50 值分别为 0.36μg/mL 和 197.60μg/mL。内皮破坏或预先用 L-NAME 处理主动脉环，将 AEMA 的 EC50 值分别从 0.36μg/mL 转移到 40.65μg/mL 和 20.20μg/mL。在存在格列本脲的情况下，M. africana 的血管舒张活性显著受到抑制。AEMA 还显著抑制了 KCl 的浓度反应曲线。口服给予 AEMA 可诱导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通过激活 NO-cGMP-ATP 依赖性钾通道途径介导，并且可能主要与其降压作用有关。
