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采用肾血管性高血压大鼠模型 (两肾一夹型 )观察海洋硫酸多糖 DPS对肾血管性高血压大鼠血清中一氧化氮 (NO)和血浆中血管紧张素 II(Ang II)及内皮素 - 1(ET- 1)含量的影响。 DPS在肾血管性高血压大鼠造模第二天起分别以 12 .50 ,2 5.0 0 ,50 .0 0 mg/ kg口服预防给药五周 ,每日给药一次。于给药前、给药后第三周和第六周分别测定动脉血压和心率。实验结束前 ,从每只大鼠取血 6 m L ,用试剂盒测定血清中 NO的含量 ;用放射免疫法测定血浆中 Ang II和 ET- 1的含量。血管紧张素转化酶抑制剂卡托普利 (14mg/ kg)作为本实验阳性对照药。结果 :DPS口服预防给药五周 ,可显著增加血清中 NO的含量和降低血浆中 ET- 1的含量 ,且呈剂量依赖性 ;DPS亦能降低血浆中 Ang II的含量 ,但未见剂量依赖性。结论 :海洋硫酸多糖 DPS对肾血管性高血压大鼠的降压作用机制可能与其促进体内 NO生成或释放、降低 AngII和 ET- 1的含量有关
Renal hypertensive rat model (two-kidney, one-clip type) observation of marine sulfated polysaccharide DPS on serum nitric oxide (NO) and plasma angiotensin II (Ang II) and endothelium in renovascular hypertensive rats Effect of Su-1 (ET-1) Content. DPS was administered prophylactically at 12.50, 25.0, and 5.00 mg/kg, respectively, for five weeks from the second day of revascularization in rats with renovascular hypertension. Arterial blood pressure and heart rate were measured before administration, on the third and sixth weeks after administration. Before the end of the experiment, blood was drawn from each rat by 6 m L. The serum NO was determined by a kit. The contents of Ang II and ET-1 in plasma were determined by radioimmunoassay. Angiotensin converting enzyme inhibitor captopril (14mg/kg) was used as a positive control drug in this experiment. Results: The oral administration of DPS for 5 weeks could significantly increase the serum NO level and decrease the plasma ET-1 content in a dose-dependent manner. DPS also reduced plasma Ang II level, but no dose dependence was found. Sex. Conclusion : The mechanism of hypotensive effect of marine sulfated polysaccharide DPS on renovascular hypertensive rats may be related to the promotion of NO production or release in vivo, and the decrease of AngII and ET-1 levels.