HO/CO通路在2K1C肾性高血压时的变化  

Changes of HO/CO pathway in renal hypertension of two-kidney one-clip hypertensive rats

作　　者：庞东卫[1] 韩莉[1] 刘俊昌[1] 马铁民[1] 徐海[1] 

机构地区：[1]北京大学医学部生理与病理生理学系,北京100083

出　　处：《中国病理生理杂志》2004年第4期556-559,共4页Chinese Journal of Pathophysiology

摘　　要：目的 :利用两肾一夹 (2K1C)高血压动物模型观察血红素加氧酶 /一氧化碳 (HO/CO)系统在高血压发病中的作用以及血红素 -L -赖氨酸 (HLL)、一氧化碳 (CO)对大鼠离体血管收缩反应性的影响 ,探讨内源性和外源性CO在高血压发生发展中的作用机制。方法 :腹腔注射HLL和CO ,观察平均动脉压 (MAP)和心率的动态变化。观察离体主动脉环对苯肾上腺素 (PHE)的反应性变化。结果 :(1)CO使 2K1C组和假手术组MAP均显著降低分别达10 0mmHg和 5 4 38mmHg(P <0 0 1) ,心率先升后降 ;HLL可使 2K1C组MAP明显降低 ,幅度为 6 1 6 7mmHg(P <0 0 1) ,心率变化不大。(2 )HLL使 2K1C组和假手术组胸主动脉环收缩反应性下降 ,并可被ZnPPⅨ所逆转。结论 :2K1C肾性高血压的产生与CO有关 ;HO/CO通路参与了肾性高血压的形成和发展。AIM: To investigate the effect of heme oxygenase /carbon monoxide(HO/CO) system on the pathogenesis of hypertension and effect of Heme-L- Lysinate(HLL), Zine protoporphyrin-IX(ZnPPIX) on vascular tension in a two kidney one-clip model. METHODS: The changes in mean arterial pressure and heart rate as well as phenylephrine(PHE)-induced contraction in isolated aortic rings of HLL, ZnPPIX- treated rats were examined after intraperitoneal administration of HLL and carbon monoxide( CO). RESULTS: (1) Injection of exogenous CO resulted in a significant decrease in mean arterial pressure in Sham and 2K1C groups(P<0.01). While HLL, the HO substrate, only reduced arterial pressure in 2K1C group. (2)HLL-induced suppression of the vasoconstriction to PHE was reversed after the vascular tissues were incubated with ZnPPIX (P<0.05). CONCLUSION: HO/CO pathway is involved in the pathogenesis of renal hypertension in two-kidney one-clip rats.

关 键 词：血红素加氧酶 一氧化碳 高血压 肾性 赖氨酸 

分 类 号：R544.14[医药卫生—心血管疾病]