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目的 探讨特异性血管紧张素Ⅱ受体 1阻断剂氯沙坦调节高血压血管内皮功能与一氧化氮合酶 (nitricoxidesynthase,NOS)的关系。 方法 采用两肾一夹型高血压大鼠(two kedney ,one cliphypertensiverat)为动物模型 ,术后第 2、 4、 6wk测血压 ,6wk后处死大鼠测血浆中NO2 -/NO3 -的含量 ,取胸主动脉作离体血管环张力实验 ,免疫印迹方法检测主动脉内皮型一氧化氮合酶 (endothelialNOS ,eNOS)及诱生型一氧化氮合酶 (inducibleNOS ,iNOS)的表达。结果 模型组大鼠相对于假手术对照组血压由 (15 83± 1 4 6 )kPa升高到 (2 3 6 7± 2 2 6 )kPa ,血浆中NO2 -/NO3 -的含量增加 (10 0 8μmol·L-1vs 37 7μmol·L-1,P <0 0 1) ,乙酰胆碱引起的最大舒张百分比下降 (73 5 %vs2 5 % ,P <0 0 1) ,主动脉中eNOS的表达降低 ,iNOS的表达增强 ;氯沙坦治疗后 ,血压、血浆中NO2 -/NO3 -的含量分别下降到 (17 5 6± 1 19)kPa、4 9 1μmol·L-1(P均 <0 0 1) ,乙酰胆碱引起的最大舒张百分比增加到 6 4 2 % ,改善主动脉中eNOS及iNOS的异常表达。结论 氯沙坦可改善两肾一夹型高血压大鼠的血管内皮功能 ,这种作用可能是通过NOS/NO途径调节的
Objective To investigate the relationship between losartan and nitric oxide synthase (NOS), a specific angiotensin Ⅱ receptor 1 blocker, in the regulation of vascular endothelial function in hypertensive rats. Methods Two kedney and one cliphypertensiverat were used as the animal models. The blood pressure was measured at the second, fourth and sixth week after the operation, and the levels of NO2 - / NO3 - in the plasma of rats were measured after 6 weeks. Thoracic aorta was used to measure the in vitro vascular ring tension. The expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) was detected by immunoblotting. Results The blood pressure of model rats increased from (15 83 ± 1 46) kPa to (23 6 7 ± 226 6) kPa and plasma NO 2 - / NO 3 - increased 8μmol·L-1vs 37 7μmol·L-1, P <0.01), the maximal relaxation percentage induced by acetylcholine decreased (73 5% vs 25%, P 0 01), the expression of eNOS in the aorta decreased, (P <0.05). After treatment with losartan, the levels of NO2 - / NO3 - in blood pressure and plasma decreased to (17 5 6 ± 1 19) kPa and 491 μmol·L -1, respectively Acetylcholine caused by the maximum percentage of diastole increased to 6242%, to improve the aorta eNOS and iNOS abnormal expression. Conclusion Losartan can improve the vascular endothelial function in two-kidney-one hypertensive rats. This effect may be mediated by the NOS / NO pathway