Lee Kyungjin, Kim Bumjung, Hur Heseung, Chinannai Khanita Suman, Ham Inhye, Choi Ho-Young
Department of Herbology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea.
Evid Based Complement Alternat Med. 2015;2015:802368. doi: 10.1155/2015/802368. Epub 2015 Oct 11.
The present study was designed to evaluate the antihypertensive effect of GaMiSamHwangSaSimTang (HVC1), a 30% ethanol extract of a mixture comprising Pruni Cortex, Scutellariae Radix, Coptidis Rhizoma, and Rhei Rhizoma, on spontaneous hypertensive rats (SHRs). The systolic blood pressure (SBP) was measured every 4 or 7 days using the noninvasive tail cuff system. The vasorelaxant effects on isolated aortic rings were evaluated. Aortic rings were contracted using phenylephrine (PE) or KCl, and the changes in tension were recorded via isometric transducers connected to a data acquisition system. In this study, oral administration of HVC1 decreased the SBP of SHRs over the experimental period. HVC1 induced concentration-dependent relaxation in the aortic rings that had been precontracted using PE or KCl. The vasorelaxant effects of HVC1 on endothelium-intact aortic rings were inhibited by pretreatment with Nω-Nitro-l-arginine methyl ester (L-NAME) or methylene blue. HVC1 inhibited the contraction induced by extracellular Ca(2+) in endothelium-denuded rat aortic rings that had been precontracted using PE or KCl. In conclusion, HVC1 reduced the SBP of SHR and relaxed isolated SHR aortic rings by upregulating NO formation and the NO-cGMP pathway and blocking the entry of extracellular Ca(2+) via receptor-operative Ca(2+) channel and voltage-dependent Ca(2+) channel.
本研究旨在评估加味三黄四逆汤（HVC1）对自发性高血压大鼠（SHR）的降压作用，HVC1是由丹皮、黄芩、黄连和大黄组成的混合物的30%乙醇提取物。使用无创尾套系统每4或7天测量一次收缩压（SBP）。评估对离体主动脉环的血管舒张作用。用去氧肾上腺素（PE）或氯化钾（KCl）使主动脉环收缩，并通过连接到数据采集系统的等长换能器记录张力变化。在本研究中，口服HVC1在实验期间降低了SHR的SBP。HVC1在使用PE或KCl预收缩的主动脉环中诱导浓度依赖性舒张。用Nω-硝基-L-精氨酸甲酯（L-NAME）或亚甲蓝预处理可抑制HVC1对内皮完整主动脉环的血管舒张作用。HVC1抑制了在使用PE或KCl预收缩的内皮剥脱大鼠主动脉环中细胞外Ca(2+)诱导的收缩。总之，HVC1通过上调NO生成和NO-cGMP途径以及通过受体操纵性Ca(2+)通道和电压依赖性Ca(2+)通道阻断细胞外Ca(2+)的进入来降低SHR的SBP并舒张离体SHR主动脉环。
