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目的 :探讨苦豆子总碱(total alkaloid of Sophora alopecuroides,TASA)降低自发性高血压大鼠(SHR)动脉血压的机制。方法 :(1)将42只16周龄的SHR随机分为SHR模型对照组、TASA组和5组拮抗剂(左旋硝基精氨酸、甲烯蓝、维拉帕米、普萘洛尔和吲哚美辛)组;另取8只同周龄Wistar大鼠作为正常对照组。TASA组:股静脉注射TASA(2、4和8 mg·kg~(-1));拮抗剂组:先分别注射对血压无影响的阻滞剂后,再给TASA(8 mg·kg~(-1));SHR组和正常组注射等量生理盐水。经颈总动脉插管记录各组给药前后的动脉血压。(2)颈动脉血压记录30 min以后,抽取正常组、SHR组和TASA组大鼠的血液2 mL,提取血清,以酶联免疫法测定各组NO、ET-1和AngⅡ的含量。结果 :(1)TASA能显著降低SHR的血压,并具有量效依赖性(SBP:r=0.83,t=56.52,P<0.01;DBP:r=0.78,t=45.92,P<0.01;MAP:r=0.83,t=54.43,P<0.01)。维拉帕米、左旋硝基精氨酸和甲烯蓝可明显抑制TASA(8 mg/kg)的降压效应(P<0.01);而吲哚美辛、普萘洛尔对TASA的作用无影响。(2)SHR组的ET-1和AngⅡ明显高于正常组,而NO低于正常组(P<0.05);TASA组的ET-1和AngⅡ显著低于SHR组,而NO则高于SHR组(P<0.05)。结论 :TASA降低SHR血压与其恢复血管内皮细胞功能释放NO的增多和减少细胞钙内流有关。
Objective: To investigate the mechanism of total alkaloid of Sophora alopecuroides (TASA) decreasing arterial blood pressure in spontaneously hypertensive rats (SHR). Methods: (1) Forty-two SHRs of 16 weeks old were randomly divided into SHR model control group, TASA group and five groups of antagonists (L-NAL, MET, Verapamil, Indomethacin) group; another eight Wistar rats of the same age as the normal control group. In the TASA group, TASA (2, 4 and 8 mg · kg -1) was injected into the femoral vein. Antagonist group was given a blocker with no effect on blood pressure, then TASA (8 mg · kg ~ (-1) -1)); SHR group and normal group were injected with the same amount of saline. Arterial blood pressure before and after administration of each group was recorded by carotid artery cannulation. (2) After the blood pressure of carotid artery was recorded for 30 min, blood was drawn from the normal group, SHR group and TASA group, and the serum was extracted. The contents of NO, ET-1 and AngⅡ were determined by enzyme-linked immunosorbent assay. Results: (1) TASA significantly reduced the blood pressure of SHR with dose-dependent (SBP: r = 0.83, t = 56.52, P <0.01; DBP: r = 0.78, t = 45.92, r = 0.83, t = 54.43, P <0.01). Verapamil, L-arginine and methylene blue significantly inhibited the antihypertensive effect of TASA (8 mg / kg) (P <0.01), while the effects of indomethacin and propranolol on TASA had no effect influences. (2) ET-1 and AngⅡ in SHR group were significantly higher than those in normal group, while NO was lower than that in normal group (P <0.05); ET-1 and AngⅡ in TASA group were significantly lower than those in SHR group (P <0.05). Conclusion: TASA reduces the blood pressure of SHR and restores the function of vascular endothelial cells to release NO and decrease the intracellular calcium influx.