Laboratorio de Hemostasia y Genética Vascular, Centro de Biofísica y Bioquímica, Instituto Venezolano de Investigaciones Científicas, Venezuela.
Phytomedicine. 2011 Apr 15;18(6):464-9. doi: 10.1016/j.phymed.2010.10.008. Epub 2010 Nov 26.
Pomolic acid has recently shown hypotensive effect in rats. The purpose of this investigation was to determine the vascular effects of this triterpenoid and to examine its mode of action. Functional experiments in rat aortic rings precontracted with norepinephrine were performed to evaluate the vasorelaxant effect of pomolic acid. This triterpenoid induced a vasorelaxation (IC₅₀ = 2.45 μM) in a concentration- and endothelium-dependent manner and showed no effect on contractions evoked by KCl (25 mM). Pre-treatment of aortic rings with L-NAME (100 μM), methylene blue (100 μM) or glibenclamide (10 μM), totally prevented the vasorelaxation induced by pomolic acid, while indomethacin (10 μM) had no effect on this response. Additionally, pomolic acid relaxation was unaffected under the muscarinic- and β-adrenergic-receptor blocked ensured for atropine and propanolol respectively (10 μM each). In contrast, the vasorelaxant effect of pomolic acid was abolished under the purinergic-receptor blocked ensured for suramin (10 μM). Finally, apyrase (0.8 U/ml) an enzyme which hydrolyses ATP and ADP did not affect pomolic acid relaxation. In summary, pomolic acid has a potent endothelium-dependent vasorelaxant effect, possibly acting through the direct activation of endothelial purinergic receptors via NO-cGMP signaling pathway, which could be part of the mechanism underlying its hypotensive effect.
齐墩果酸最近在大鼠中表现出降压作用。本研究旨在确定这种三萜的血管作用，并研究其作用机制。通过预先用去甲肾上腺素收缩的大鼠主动脉环进行功能实验，评估齐墩果酸的血管舒张作用。这种三萜以浓度和内皮依赖性方式诱导血管舒张（IC₅₀ = 2.45 μM），对 KCl（25 mM）引起的收缩无影响。用 L-NAME（100 μM）、亚甲蓝（100 μM）或格列本脲（10 μM）预处理主动脉环，完全阻止了齐墩果酸引起的血管舒张，而吲哚美辛（10 μM）对这种反应没有影响。此外，在确保分别用阿托品和普萘洛尔（各 10 μM）阻断毒蕈碱和 β-肾上腺素能受体的情况下，齐墩果酸的舒张作用不受影响。相比之下，在确保用苏拉明（10 μM）阻断嘌呤能受体的情况下，齐墩果酸的血管舒张作用被消除。最后，水解 ATP 和 ADP 的酶，即 apyrase（0.8 U/ml），不影响齐墩果酸的舒张作用。总之，齐墩果酸具有强大的内皮依赖性血管舒张作用，可能通过 NO-cGMP 信号通路直接激活内皮嘌呤能受体发挥作用，这可能是其降压作用的机制之一。
