金鸡菊有效部位对高血压小鼠的血压和肾素-血管紧张素系统的影响

目的观察金鸡菊提取物70%乙醇洗脱物对高血压小鼠血压、血浆血管紧张素Ⅰ（AngⅠ）、血浆血管紧张素Ⅱ（AngⅡ）和组织中AngⅡ浓度的影响。方法采用高盐（80mg/mLNaCl溶液）冷激法,连续20d,形成小鼠高血压模型;将实验小鼠分为正常组、模型组、卡托普利组（40mg/kg）和金鸡菊提取物70%乙醇洗脱物低、中、高剂量（40、80、160mg/kg）组。连续ig给药28d后,采用颈动脉插管法测定小鼠血压并取血,放射免疫法测定血浆AngⅠ、AngⅡ、及肾组织中AngⅡ的含量。结果模型组血浆AngⅠ和组织中AngⅡ含量均明显高于正常组（P〈0.05）,其血压和血浆AngⅡ含量显著高于正常组（P〈0.01或P〈0.001）;与模型组相比,金鸡菊提取物70%乙醇洗脱物中、高剂量（80、160mg/kg）组血浆AngⅠ含量明显升高（P〈0.05）,血浆AngⅡ含量极显著降低（P〈0.001）,肾组织中的AngⅡ含量显著降低（P〈0.01）。结论金鸡菊提取物70%乙醇洗脱物可明显升高AngⅠ水平,减少AngⅡ生成,推测其降压机制主要是通过影响肾素–血管紧张素系统,发挥AngⅠ拮抗剂或血管紧张素转化酶抑制剂的作用。

Effect of Coreopsis tinctoria effective fraction on blood pressure and renin-angiotensin system in hypertensive mice

Objective To observe the effect of 70% ethanol elution of Coreopsis tinctoria extract （EECTE） on blood pressure, the concentration of angiotensin I （Ang I） and angiotensin Ⅱ（Ang Ⅱ） in plasma, and the concentration of Ang Ⅱ in tissue of hypertensive mice. Methods The hypertension model of mice was established by ig giving high-salt water and keeping them in low-temperature environment for 4 h daily for 20 d; The mice were divided into control, model, Captopril （40 mg/kg）, low-, mid-, and high-dose （40, 80, and 160 mg/kg） EECTE groups. After ig administration for 28 d, the blood pressure was measured, the blood and kidney tissue were collected, and the plasma concentration of Ang I, Ang Ⅱ, and tissue homogenate Ang II were determined by radioimmunoassay. Results The Ang I level in plasma and Ang Ⅱ level in tissue homogenate in model group were obviously higher than those in the control group （P 〈 0.05）, and the blood pressure and concentration of plasma Ang II were significantly higher than those in the control group （P 〈 0.01, 0.001）. The mid- and high-dose EECTE increased Ang I and reduced Ang II in plasma obviously （P 〈 0.01）, and lessened local Ang Ⅱ in tissue homogenate compared with those in the model group （P 〈 0.001）. Conclusion EECTE may increase Ang I and reduce Ang Ⅱ markedly, so the possible mechanism in the reduction of blood pressure in hypertensive mice is due to its effect on renin-angiotensin system and the effect ofAng I antagonist or angiotensin converting enzyme inhibitor.