ABNORMAL WATER METABOLISM IN TYPE 1A ANGIOTENSIN RECEPTOR DEFICIENT MICE

肾乳头的长度决定了尿液的浓度 容量。血管紧张素II(A II)可能在发育和发育中发挥作用 乳头闭锁所提示的乳头的维持 在缺乏A的基因敲除小鼠中发现的II.这一疾病的发病机制 乳头状性闭锁尚不清楚。它还没有被 AT1a[Agtr1a]或AT2AII受体基因对MIXED的干扰 遗传背景，尽管Agtr1A(-/-)小鼠有一个集中的 叛逃。具有97%C57BL/6遗传背景的AT1a缺陷小鼠 [B6Agtr1A(-/)]在4个月龄时有集中缺陷，并且 8个月后出现乳头状闭锁。排除细微乳头 Agtr1a(-/-)小鼠的异常及时程检测 B6Agtr1a(-/-)的乳头状改变已经很难使用 标准方法。我们建议使用MRM来更好地显示肾脏 这些小鼠模型中的乳头状结构

The length of the renal papilla determines urinary concentrating capacity. Angiotensin II (A II) may play a role in development and maintenance of the papilla, as suggested by the papillary atresia found in knockout mice lacking A II. the pathogenesis of this papillary atresia is not understood. It has not been reproduced by disruption of either AT1A [Agtr1A] or AT2 A II receptor genes on mixed genetic backgrounds, although Agtr1A (-/-) mice have a concentrating defect. AT1A deficient mice with a >97% C57 BL/6 genetic background [B6Agtr1A (-/)] have a concentrating defect at 4 months of age, and develop papillary atresia by 8 months. Exclusion of subtle papillary abnormalities in Agtr1A (-/-) mice, and examination of the time course of the papillary changes to B6Agtr1A (-/-) has been difficult using standard methods. We propose to use MRM to better visualize the renal papillary in these mouse models