ABNORMAL WATER METABOLISM IN TYPE 1A ANGIOTENSIN RECEPTOR DEFICIENT MICE

肾乳头的长度决定尿的浓缩 容量 血管紧张素II（A II）可能在发育中起作用， 维持乳头，如乳头闭锁所示 在缺乏A II的基因敲除小鼠中发现。 的发病机制 乳头状闭锁还不清楚。 它没有被复制， AT 1A [Agtr 1A]或AT 2 A II受体基因的破坏 遗传背景，尽管Agtr 1A（-/-）小鼠具有集中的 缺损 具有>97% C57 BL/6遗传背景的AT 1A缺陷型小鼠 [B6 Agtr 1A（-/）]在4个月大时有集中缺陷，并且 8个月时出现乳头状闭锁。 隐蔽乳头状排斥 Agtr 1A（-/-）小鼠的异常，以及时间过程的检查 B6 Agtr 1A（-/-）的乳头状变化难以使用 标准方法。 我们建议使用MRM更好地显示肾脏 在这些小鼠模型中，

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