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NO/HO-1参与ACEI对抗大鼠血管氧化作用

Nitric oxide/heme oxygenase-1 mediates the antioxidant effect of ACEI in rat aortic rings

目的:研究血管紧张素转换酶抑制剂(ACEI)对抗过氧化氢(H2O2)引起的血管收缩功能下降,并分析其抗氧化机制是否通过诱导血色素氧化酶-1(HO-1),以及一氧化氮(NO)在其中的作用.方法:采用血管环灌流装置,观察大鼠胸主动脉环的收缩效应.结果:①经300 μmol/L H2O2孵育血管15 min后,主动脉环对苯肾上腺素(PE)引起的血管收缩反应下降;卡托普利(含巯基的ACEI)和培哚普利(不含巯基的ACEI)孵育1 h后可对抗H2O2引起的血管收缩反应下降.②ACEI可使血管HO-1活性增加;用锌原卟啉IX(ZnPP IX)抑制HO-1的活性后,卡托普利抗H2O2损伤的作用被阻断;HO-1诱导剂高铁血红素及其产物胆红素亦能模拟卡托普利的抗H2O2损伤作用.③NOS抑制剂左旋硝基精氨酸甲酯(L-NAME)和GC抑制剂亚甲蓝均可取消卡托普利的血管保护作用.④用亚硝基乙酰青霉胺(SNAP)孵育血管30 min,可对抗H2O2引起的血管收缩反应下降,而ZnPP IX可取消SNAP的血管保护作用.结论:含有和不含巯基的ACEI均具有对抗H2O2引起的血管收缩功能下降的作用,其主要机制可能是通过引起NO产生增加和诱导HO-1而实现的.

作 者:
朱立 沈岳良 徐和靖 汪洋 陈莹莹  
作者单位:
朱立,沈岳良,陈莹莹(浙江大学医学院,生理学系,浙江,杭州,310058)
徐和靖,汪洋(温州医学院,生理教研室,浙江,温州,325027) 
刊 名:
浙江大学学报(医学版)  ISTIC PKU
英文刊名:
JOURNAL OF ZHEJIANG UNIVERSITY(MEDICAL SCIENCES) 
年,卷(期):
2007 36(1) 
分类号:
R331.3 
关键词:
氧化还原酶类 知识脉络  过氧化氢 知识脉络  血管紧张素转换酶抑制药/药理学 知识脉络  一氧化氮 知识脉络  血管收缩/药物作用 知识脉络 
机标分类号:
O61 R96 
机标关键词:
对抗大鼠血管血管收缩反应卡托普利血管保护作用血管紧张素转换酶抑制剂左旋硝基精氨酸甲酯主动脉环亚硝基乙酰青霉胺收缩功能血色素氧化酶巯基孵育高铁血红素苯肾上腺素一氧化氮氧化机制锌原卟啉损伤作用收缩效应 
基金项目:
浙江省自然科学基金,浙江省教育厅资助项目 
DOI:
 
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