内皮舒张因子与血管紧张素Ⅱ之间调控关系的动物实验研究

Animal Experimental Study between the EDRF/NO And Angiotensin Ⅱ in Regulative Relations

目的探讨内皮舒张因子(EDRF/NO)和血管紧张素Ⅱ(Angiotensin Ⅱ,AngⅡ)之间的调控关系。方法在设置整体和离体大鼠主动脉灌流模型上,进行相关因素灌流,观察血浆AngⅡ水平、组织环一磷酸鸟苷(cGMP)含量和血管AngⅡ释放量的动态变化。结果整体实验结果显示:静脉滴注AngⅡ使主动脉cGMP含量较对照组显著增加(P<0.01);滴注L-NNA使主动脉cGMP较对照组显著减少(P<0.01),血浆AngⅡ-ir显著增加(P<0.01);联合滴注L-NNA和AngⅡ组,与滴注L-NNA比较,主动脉cGMP无明显变化,而血浆AngⅡ-ir显著增加(P<0.01)。离体结果显示:AngⅡ灌流血管条cGMP含量,较对照组明显增加(P<0.01);Ach灌流显著增加cGMP水平(P<0.01),则减少血管AngⅡ-ir的释放(P<0.01);L-NNA灌流使血管cGMP含量显著降低(P<0.01),AngⅡ释放量较明显增加(P<0.01);MB灌流使血管cGMP含量明显下降(P<0.01),则对AngⅡ释放量无明显影响。结论AngⅡ可能通过自分泌方式促使EC释放EDRF/NO,EDRF/NO既拮抗AngⅡ的生物学效应,又对AngⅡ起着负反馈调节作用。

Objective To probe into modulation effect between the EDRF/NO And Ang Ⅱ. Methods In the whole Wister rat and rat＇ s aorta perfusion model , they are carried through relative factors so that dynamic changes of plasm Ang Ⅱ - ir, cGMP level of tissue and vascular Ang Ⅱ release level are observed. Results Whole Wister rat＇ s experiment results： In Ang Ⅱ group, the aortic cGMP content is markedly elevated compared with group control （ P 〈 0.01 ） ; In L - NNA group , With control group comparison , the GMP level is markedly reduced （ P 〈 0.01 ） , plasm Ang Ⅱ - ir is markedly elevated （ P 〈 0.01 ） ; In the L - NNA ＋ Ang Ⅱ group, compared with L - NNA ,the cGMP content is not too obviously increases while plasm Ang Ⅱ - ir is markedly elevated （ P 〈 0.01 ）. Experiment results of aorta perfusion model： AngⅡ perfusion causes the vascular ring cGMP content is markedly elevated , With control group comparison ; With Ach perfusion, cGMP content is markedly increased （P〈0.01 ） while vascular Ang Ⅱ - ir release is decreased （ P 〈 0.01 ） ; L- NNA perfusion causes the vascular cGMP content is markedly reduced but the release of Ang Ⅱ is obviously increased （P 〈 0.01 ） ; With MB perfusion, causes cGMP content to be markedly drceased（P 〈0.01 ） ,but it do not affect release of Ang Ⅱ. Conclusions These resuits susgest that Ang Ⅱ promotes EC to release EDRF/NO by autocrine. EDRF/NO may inhibit Ang Ⅱ biological effect and also is getting up the negative feedback control action to Ang Ⅱ.