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目的 :研究尾加压素Ⅱ (urotensinⅡ ,UⅡ )对大鼠主动脉一氧化氮合酶 (nitricoxidesynthase ,NOS) /一氧化氮 (nitricoxide,NO)系统的影响。方法 :体外血管薄片孵育 ,以生化及放射活性分析方法分别测定孵育液中亚硝酸盐 (NO-2 )含量 ,血管NOS活性及cGMP含量。结果 :孵育 1.5h到 3h ,UⅡ (10 -9～ 10 -7mol·L-1)呈浓度依赖地刺激血管NO-2 生成增加 (14.8%～ 80 .9% )。UⅡ刺激血管组织总NOS和固有型NOS活性显著增加 (P <0 .0 5或P <0 .0 1)而不影响iNOS活性 (P >0 .0 5 )。 10 -9～ 10 -7mol·L-1的UⅡ呈浓度依赖的增加血管组织cGMP含量 (P <0 .0 1)。实验还观察到NOS抑制剂左旋硝基精氨酸 (GN L nitro arginine ,L NNA)显著抑制了UⅡ刺激的血管组织NOS激活、NO生成和cGMP含量增加。结论 :UⅡ激活血管组织NOS/NO途径 ,增加血管NO生成与cGMP含量
Objective: To investigate the effect of urotensin Ⅱ (UⅡ) on the nitric oxide synthase (NOS) / nitric oxide (NO) system in rat aorta. Methods: The in vitro vascular slices were incubated. The content of nitrite (NO-2), the activity of NOS and the content of cGMP in blood were measured by biochemical and radioactive assay. Results: UⅡ (10 -9 -10 -7 mol·L -1) stimulated NO-2 production in a concentration-dependent manner (14.8% -80.9%) after 1.5h to 3h incubation. UII stimulated the total NOS and NOS activity of vascular tissue significantly increased (P <0.05 or P <0.01) and did not affect iNOS activity (P> 0.05). The UⅡ concentration of 10 -9 -10 -7 mol·L -1 increased the concentration of cGMP in vascular tissue in a concentration-dependent manner (P <0.01). It was also observed that NOS inhibitor L-NNA significantly inhibited NOS activation, NO production and cGMP content in blood vessels stimulated by UII. CONCLUSION: UⅡ activates NOS / NO pathway in vascular tissue and increases NO production and cGMP content in blood vessels