摘要
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-
The effects of D-polymannuronic sulfate (DPS) on the serum nitric oxide levels and plasma Endothelin-1 and Angiotensin II contents were studied in renovascular hypertensive rats [two-kidney one clip, Goldblatt (2-K 1C)]. In the prophylactic experiment in which the effects of DPS given orally at doses of 12.50, 25.00 and 50.00 mg/kg once daily for five weeks simultaneously with the initiation of the establishment of renovascular hypertensive model were evaluated. Serum nitric oxide (NO) was determined with nitric oxide kit while plasma Angiotensin II (Ang II) and Endothelin-1 (ET-1) were measured by radioimmunoassay. Captopril (14 mg/kg), an Angiotensin II inhibitor, was served as a positive agent. The results showed that DPS could produce a dose-dependent effect on increased serum nitric oxide levels and decreased Endothelin-1 contents, whereas the inhibitory effect of DPS on plasma Angiotensin II contents was not found in a dose-dependent manner. It implicates that the mechanisms underlying the antihypertensive effects of DPS might be associated with its actions on increasing the synthesis or release of NO and decreasing the production of Ang II and ET-1 in vivo.
出处
《青岛海洋大学学报（自然科学版）》
CSCD
北大核心
2001年第2期179-184,共6页
Journal of Ocean University of Qingdao
基金
国家"九五"科技攻关项目 !(96 - C0 2 - 0 1)&&
