Facultad de Farmacia, Universidad Autónoma del Estado de Morelos, Avenida Universidad 1001, Col. Chamilpa, 62209, Cuernavaca, Morelos, México.
J Pharm Pharmacol. 2010 Sep;62(9):1167-74. doi: 10.1111/j.2042-7158.2010.01146.x.
The aim was to evaluate the relaxant effect of extracts from Valeriana edulis and determine the possible mechanism of action of the hexanic extract as vasorelaxant agent.
Extracts from rhizomes obtained by maceration (hexanic (HEVe), dichloromethanic (DEVe), methanolic (MEVe) and hydroalcoholic (HAEVe) (3.03-500 microg/ml)) were evaluated on aortic rat rings with and without endothelium.
Extracts induced a significant concentration-dependent and endothelium-independent relaxation on isolated rat aorta pre-contracted with noradrenaline (0.1 microM). HEVe, the most potent extract (0.15-50 microg/ml), induced relaxation in aortic rings pre-contracted with KCl (80 mM), with an IC50 value of 34.61 +/- 1.41 microg/ml and E(max) value of 85.0 +/- 4.38%. Pretreatment with HEVe (30 microg/ml) also inhibited contractile responses to noradrenaline and CaCl(2). HEVe (9.98 +/- 2.0 microg/ml) reduced noradrenaline-induced transient contraction in Ca(2+)-free solution, and inhibited contraction induced by KCl (80 mM). In endothelium-denuded rings, the vasorelaxant effect of HEVe was not modified by 1-H-[1,2,4]-oxadiazolo-[4,3a]-quinoxalin-1-one (1 microM), tetraethylammonium (5 mM), glibenclamide (10 microM) or 2-aminopyridine (100 microM).
Our results suggest that HEVe induces relaxation through an endothelium-independent pathway, involving blockade of Ca(2+) channels, and this effect could be related to the presence of valepotriates.
评估缬草属植物提取物的舒张作用，并确定正己烷提取物作为血管舒张剂的可能作用机制。
通过浸渍法从根茎中获得提取物（正己烷（HEVe）、二氯甲烷（DEVe）、甲醇（MEVe）和水醇（HAEVe）（3.03-500 μg/ml）），并在有或没有内皮的情况下评估其对大鼠主动脉环的作用。
提取物在去甲肾上腺素（0.1 μM）预收缩的大鼠离体主动脉上引起浓度依赖性和内皮非依赖性的显著舒张。HEVe 是最有效的提取物（0.15-50 μg/ml），在 KCl（80 mM）预收缩的主动脉环中诱导舒张，IC50 值为 34.61 ± 1.41 μg/ml，E(max) 值为 85.0 ± 4.38%。HEVe（30 μg/ml）预处理也抑制了去甲肾上腺素和 CaCl2 引起的收缩反应。HEVe（9.98 ± 2.0 μg/ml）减少了 Ca2+ 游离溶液中去甲肾上腺素引起的短暂收缩，并抑制了 KCl（80 mM）引起的收缩。在内皮去极化的环中，HEVe 的血管舒张作用不受 1-H-[1,2,4]-恶二唑-[4,3a]-喹喔啉-1-酮（1 μM）、四乙铵（5 mM）、格列本脲（10 μM）或 2-氨基吡啶（100 μM）的影响。
我们的结果表明，HEVe 通过一种内皮非依赖性途径诱导舒张，涉及钙通道的阻断，这种作用可能与缬草酸酯的存在有关。
