一氧化氮改变肾性高血压大鼠主动脉功能

Nitric oxide changes aortic function in rats with renal hypertension 

探讨一氧化氮 (NO)对二肾一夹 (2K1C)肾性高血压大鼠主动脉功能的影响。实验分为 5组 :假手术、2K1C、卡托普利 (captopril)、NAME(Nω Nitro L argininemethylester)和精氨酸组。结果显示 :在 2K1C组 ,大鼠手术后4周的平均动脉压显著升高 ,主动脉对ACh的舒张反应明显减弱 ,对苯肾上腺素的收缩反应明显增强 ,主动脉壁环鸟苷酸 (cGMP)含量显著减少。卡托普利可完全逆转 2K1C组大鼠的上述改变。L 精氨酸能使 2K1C大鼠异常的主动脉反应性部分恢复 ,主动脉壁的cGMP含量显著升高。用一氧化氮合酶抑制剂L NAME处理 2K1C大鼠 ,血压进一步升高 ,主动脉对ACh的舒张反应进一步减弱 ,cGMP含量减少 ,而苯肾上腺素的收缩反应未受明显影响。结果提示 :2K1C肾性高血压大鼠的主动脉内皮功能失调与NO生成和释放减少、肾素 血管紧张素系统活性增强有关 ,这些因素可能参与 2K1C大鼠高血压的发生和维持。

This work was undertaken to investigate the effect of nitric oxide (NO) on aortic function of two kidney and one clip (2K1C) rats with renal hypertension. Animals were divided into 5 groups: the sham operation, 2K1C, captopril, L arginine and L NAME groups. The results are as follows. At the 4th week after con^striction of the left renal artery, the mean arterial pressure was significantly elevated. In isolated aortic rings, acetylcholine induced dilation was attenuated, and phenylephrine induced contractile response was markedly enhanced. The level of aorta cGMP content was significantly lowered. These changes were abolished in 2K1C rats treated with captopril. L arginine partially reversed the aortic vascular reactivity of 2K1C rats, and elevated aortic cGMP content. In 2K1C rats treated with nitric oxide synthase inhibitor, L NAME, blood pressure was increased further, acetylcholine induced aorta diastolic response was attenuated further and cGMP content reduced, while phenylephrine induced contractile response was unaffected. These results suggest that deficiency of nitric oxide production and increase in renin angiotensin system activity may contribute to vascular endothelial dysfunction of 2K1C rats, and these factors may be involved in development and maintenance of 2K1C renal hypertension.