<International Circulation>：Are there any non-ACE dependent biosynthetic pathways of antiotensin II? If so， can we use this to develop some new RAS antagonistic drugs?

  《国际循环》：最后一个问题。您认为脂肪组织中是否存在非血管紧张素酶依赖的血管紧张素II合成的途径呢？如果存在，是否有助于开发新的RAS 拮抗剂？

    Prof. Cassis:There is data from another laboratory that there is production of angiotensin II from angiotensin I~XII but I think that it is still ACE dependent. We are using a model that we have developed where we do not have angiotensinogen and we are then looking at the different peptides that are reduced in that model to try to get at those questions and learn if is all angiotensinogen doing giving rise to angiotensin II and is it through the traditional pathway. I think there are some possibilities there but if you block renin or ACE in most of the mouse models we use， you get profound effects to reduce cardiovascular diseases. Thus， it appears the classical system is the most important system.

    Cassis教授：其它实验室研究数据表明，脂肪组织存在某种物质可减少血管紧张素原2转换成血管紧张素1-12，至于其是否是ACE依赖性，我并不清楚，我想其应该是依赖的。我们正在通过我们建立的无angiten cinnagen 表达的小鼠模型寻找特异性肽类，以期解决上述问题。“angiten cinnagen自身可直接升高血管紧张素原2，还是通过传统途径？” 我想这存在一定可能性，但说实话，如果阻断模型小鼠的肾素或ACE通路，就能显著降低心血管疾病的发生率。因此，经典的传统通路似乎是最重要的系统。

    <International Circulation>：Thank you professor Cassis.
  《国际循环》：谢谢Cassis教授。

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