Faculty of Pharmaceutical Sciences, Hoshi University, Shinagawa-ku, Tokyo, Japan.
J Nat Med. 2013 Jan;67(1):196-201. doi: 10.1007/s11418-012-0644-0. Epub 2012 Mar 3.
A cyclic depsipeptide, FR900359, isolated from Ardisia crenata was evaluated for vasorelaxant effects on rat aortic arteries. FR900359 caused concentration-dependent relaxation (1 nM-10 μM) in phenylephrine-precontracted endothelium-intact aortic rings, which was inhibited by addition of L-NMMA, a NOS inhibitor. In endothelium-denuded rings, the relaxant effect of low concentrations of FR900359 was diminished, but remained at high concentrations. In endothelium-denuded rings, FR900359 at 0.1 μM significantly attenuated high-K(+)-induced contractions and completely inhibited Ca(2+)-induced contractions. These results suggest that the vasorelaxant effect of FR900359 is mediated through the increased release of NO from endothelial cells at low concentrations, and can be attributed to inhibitory effects on voltage-dependent Ca(2+) channel- and receptor-operated Ca(2+) channel-dependent Ca(2+) influx at high concentrations.
从紫金牛属植物中分离得到的环二肽 FR900359 被评估其对大鼠主动脉的血管舒张作用。FR900359 引起苯肾上腺素预收缩的内皮完整的主动脉环浓度依赖性舒张（1 nM-10 μM），NOS 抑制剂 L-NMMA 可抑制其舒张作用。在内皮剥脱的环中，低浓度 FR900359 的舒张作用减弱，但在高浓度时仍存在。在内皮剥脱的环中，FR900359 在 0.1 μM 时显著减弱高 K + 诱导的收缩，并完全抑制 Ca 2 + 诱导的收缩。这些结果表明，FR900359 的血管舒张作用是通过低浓度时内皮细胞中一氧化氮（NO）释放增加介导的，并且可以归因于高浓度时对电压依赖性 Ca 2 + 通道和受体操纵的 Ca 2 + 通道依赖性 Ca 2 + 内流的抑制作用。
