Vasodilation by banhabackchulchunmatang, a Chinese medicine, is associated with negative modulation of PKCα activation and NO production
Vasodilation by banhabackchulchunmatang, a Chinese medicine, is associated with negative modulation of PKCα activation and NO production
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DOI：
10.1016/j.lfs.2003.06.040
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发表时间：
2003-12-26
期刊：
影响因子：
6.1
通讯作者：
Morgan, KG
中科院分区：
文献类型：
--
作者：
Shin, HM;Morgan, KG
班哈巴克楚春玛汤（BCT）是一种广泛使用的具有血管扩张作用的草药。在本研究中，我们研究了其血管作用的亚细胞机制。在存在和不存在内皮细胞的情况下，BCT放松血管条预收缩苯肾上腺素，但松弛的幅度更大的内皮细胞的存在。NOS抑制剂L-NAME或cGMP抑制剂亚甲蓝均可抑制这种舒张作用，表明NO参与了舒张过程。NO的参与得到了BCT存在下人脐静脉内皮细胞亚硝酸盐形成增加的支持。在血管条中，BCT降低了20 kDa肌球蛋白轻链的磷酸化水平。BCT也直接抑制苯肾上腺素诱导的蛋白激酶Calpha（PKCalpha）易位在新鲜分离的单个雪貂门静脉平滑肌细胞。总之，这些作用可能有助于BCT的血管舒张作用。(C)2003年爱思唯尔公司All rights reserved.
Banhabackchulchunmatang (BCT) is a widely used herbal medicine with vasodilatory actions. In the present study, we investigated the subcellular mechanisms of its vascular actions. Both in the presence and absence of endothelium, BCT relaxed vascular strips precontracted with phenylephrine, but the magnitude of relaxation was greater in the presence of endothelium. The relaxation was inhibited by either L-NAME, an NOS inhibitor, or methylene blue, a cGMP inhibitor, indicating the involvement of nitric oxide (NO). The involvement of NO was supported by the increased formation of nitrite from human umbilical vein endothelial cells in the presence of BCT. In vascular strips, BCT lowered the phosphorylation level of the 20 kDa myosin light chains. BCT also directly inhibited phenylephrine-induced protein kinase Calpha (PKCalpha) translocation in freshly isolated single ferret portal vein smooth muscle cells. Together, these effects are likely to contribute to the vasodilatory actions of BCT. (C) 2003 Elsevier Inc. All rights reserved.