摘要
目的:观察一氧化氮(ＮＯ)和血管紧张素Ⅱ(ＡｎｇⅡ)在压力超负荷心肌肥大反应过程中的作用。方法:利用腹主动脉缩窄性高血压大鼠模型,测量平均动脉压(ＭＡＰ)和左心室质量/体质量比值(ＬＶＷ/ＢＷ)。结果:在ＳＤ乳鼠腹主动脉缩窄性高血压模型中,ＭＡＰ和ＬＶＷ/ＢＷ呈时间依赖性增高,从术后第１周开始ＭＡＰ和ＬＶＷ/ＢＷ均明显增高,至第８周达高峰;ＮＯ前体Ｌ－Ａｒｇ和ＡｎｇⅡ１型受体(ＡＴ１)拮坑剂芦沙坦(Ｌｏｓ),明显阻断腹主动脉缩窄性高血压大鼠的ＭＡＰ和ＬＶＷ/ＢＷ的增高效应;用ＮＯＳ抑制剂ＮＧ－硝基左旋精氨酸甲酯(Ｌ－ＮＡＭＥ)同时处理假手术组(Ｓｈａｍ)和腹主动脉缩窄性(ＣＯＡ)高血压组大鼠,ＭＡＰ和ＬＶＷ/ＢＷ均进一步增高。结论:ＡｎｇⅡ参与诱发压力超负荷高血压和心肌肥大反应的发生;ＮＯ具有抑制压力超负荷引起的高血压和心肌肥大反应。
To investigate the effects of nitric oxide (NO) and angiotensin Ⅱ on myocardial hypertrophy caused by overloaded pressure. Method: The coarctation of the abdominal aorta (COA) hypertension model was established in Spragrue-Dawley rats. The mean arterial pressure (MAP) and the ratio of left ventricular weight to body weight (LVW/BW) were measured in each rat. Results: The MAP and LVW/BW were significantly increased at week 1,4,8, and 12 with tis peak at week 8 after COA, Both NO precursor, L-Arg and angiotensin Ⅱ type one receptor (AT1) antagonist losartan (Los) and significantly blocked the in crease in MAP and LVW/BW cause by COA. In contrast, MAP and LVW/BW were increased further after the rats received NOS antagonist L-NAME in both sham and COA groups. Conclusion: Ang Ⅱ participats in the development of hypertension and myocardial hypertrophy induced by COA while NO may have the opposite effect.
出处
《海南医学院学报》
CAS
2002年第1期1-4,12,共5页
Journal of Hainan Medical University
基金
海南省自然科学基金(NO.30018)
省卫生厅资助课题(NO
琼卫2000-78)
