内源性一氧化碳在大鼠高血压发病中的作用(英文)  

ROLE OF ENDOGENOUS CARBON MONOXIDE IN HYPERTENSION PATHOGENESIS OF RATS

作　　者：欧和生[1] 杨军[1] 董林旺[1] 庞永正[1] 苏静怡[1] 唐朝枢[1] 刘乃奎[1] 

机构地区：[1]北京医科大学心血管研究所,北京100083

出　　处：《生理学报》1998年第6期643-648,共6页Acta Physiologica Sinica

基　　金：国家自然科学基金!39730220

摘　　要：本实验研究内源性血红素氧化酶（hemeOxygenase，HO）／一氧化碳（CO）系统在大鼠高血压发病中的作用。2，4-二甘油次卟啉锌（ZnDPBG）是体内HO活性抑制剂。用ZnDPBG处理大鼠后，检测其血压和血浆肾上腺素、去甲肾上腺素、内皮素、硝酸盐和亚硝酸盐、6-酮-PGF1a的改变，同时测定主动脉平滑肌中HO活性和CO的生成。此外还观察了CO和HO底物血红素-左旋赖氨酸盐（heme－L－lysinate，HIL）对HO抑制性大鼠和自发性高血压大鼠血压的影响。结果发现：ZnDPBG使大鼠血浆肾上腺素、去甲肾上腺素、内皮素和一氧化氮代谢产物含量明显增加，同时动脉血压升高；主动脉平滑肌HO活性和CO产生明显受到抑制。CO能使HO抑制性大鼠平均动脉压（MABP）明显降低，HLL则无此效应。在高血压大鼠，CO或HLL均能导致其MABP急性降低。本实验提示HO／CO系统在体内有抗高血压生物学效应，内源性CO在血管张力调节和高血压发生的机制中具有重要作用。The present study investigated the contribution of endogenous heme oxygenase (HO)/carbon monoxide (CO) system to hypertension pathogenesis of rats. rats.Zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO), was used to inhibit HO activity in vivo It was found that the blood pressure of rats with HO inhibition was significantly elevated, and plasma levels of adrenaline, noradrenaline, endothelin, nitrate and nitrite were significantly increased. HO activity and HbCO formation within vascular smooth tissues were significantly inhibited after administration of Furthermore,administration of exogenous CO into HO inhibiting rats led to MABP decrease, but injection of HO substrate, heme-Llysinate, had no effect on HO inhibition-induced hypertension In spontaneously hypertensive rats, injection of exogenous CO resulted in a significant decrease of MABP, and heme-L-lysinate had a similar effect with exogenous CO. These data show that HO/CO system has an anti-hypertension bilogical action, suggesting that endogenous CO plays an important role in hypertension pathogenesis

关 键 词：高血压 一氧化碳 血红素氧化酶 发生机制 

分 类 号：R544.1[医药卫生—心血管疾病]