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

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Biotechnology Resource Grants (P41)
Project #
3P41RR005959-09S1
Application #
6122323
Study Section
Project Start
1999-02-01
Project End
1999-08-31
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
9
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Duke University
Department
Type
DUNS #
071723621
City
Durham
State
NC
Country
United States
Zip Code
27705
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