尾加压素Ⅱ对大鼠主动脉一氧化氮合酶/一氧化氮系统的影响  

Effect of urotensin Ⅱ on nitric oxide synthese/nitric oxide pathway in rat aorta

作　　者：姜志胜[1] 张勇刚[1] 齐永芬[1] 许松[2] 徐少平[3] 庞永政[1] 唐朝枢[1] 

机构地区：[1]北京大学第一医院心血管病研究所科,北京100034 [2]北京大学第一医院中心实验室，北京 100034 [3]中国人民解放军北京军区总医院心内科

出　　处：《北京大学学报（医学版）》2001年第2期147-149,共3页Journal of Peking University:Health Sciences

基　　金：国家自然科学基金重点项目 (3 973 0 2 2 0 )

摘　　要：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 。SUMMARY Objective: To study the effect of urotensin(U Ⅱ) on nitric oxide synthase(NOS)/nitric oxide(NO) system in rat aorta. Methods: The aortic slices were incubated in vitro. The medium nitrite content, vascular NOS activities and cGMP content were measured. Results: After incubation of aorta for 1.5-3.0 h, UⅡ(10 -9 -10 -7 mol·L -1 ) increased nitrite production ( 14.8%- 80.9% , P <0.01) in dose dependent manner. U Ⅱ significantly stimulated the total NOS activities, mainly activated constitutive NOS ( P <0.05 or P <0.01), however, the inducible NOS activities were not altered ( P >0.05). Incubation of aortic slices with U Ⅱ (10 -9 -10 -7 mol·L -1 ) increased vascular cGMP content in dose dependent manner. Co incubation vascular tissue with U Ⅱ and GN L nitro arginine, an inhibitor of NOS, obviously inhibited the U Ⅱ induced NOS activation, NO production and cGMP formation. Conclusion: The results suggest that U Ⅱ can activate the vascular NOS/NO pathway, increasing tissue NO production and cGMP content.

关 键 词：尾加压素Ⅱ 一氧化氮合酶 一氧化氮 代谢 血管升压素 药理学 主动脉 

分 类 号：R972[医药卫生—药品]