| Official Name |
C57BL/6-Bdkrb1/Bdkrb2tm2Mki/J |
| Description |
Publications report that mice homozygous for targeted
mutations in the tandem bradykinin B1 and B2 receptors,
commonly referred to as B1RB2R -/-, are viable, fertile and
display no major defects. At 4 months of age,
non-manipulated B1RB2R -/- mice exhibited no significant
differences in blood pressure or kidney function when
compared to mice deficient only in the B2 receptor. Fasted
B1RB2R -/- mice exhibited significantly lower levels of
plasma nitrite/nitrate compared to Bdkrb2 deficient mice.
Post-ischemic B1RB2R -/- mice exhibited significantly higher
plasma levels of urea nitrogen and creatinine, higher levels
of oxidative nuclear and mitochondrial DNA modification, and
increased rates of apoptosis and mortality than either
wildtype or Bdkrb2 deficient mice. Histological evaluation
of the kidney showed that post ischemic B1RB2R -/- mice
exhibit more severe histological changes in the renal
proximal tubules than either wildtype or Bdkrb2 deficient
mice (Kakoki et al, 2007). The Ins2Akita mutation was
introduced by cross with the B6- Ins2Akita stock to assess
the effect of chronic diabetes on complications development
in The Jackson Laboratory vivarium. In B1RB2R -/- male but
not female mice, mean albumin/creatinine ratio (ACR) in
urine was modestly elevated at 25 weeks of age. However, no
significant renal histopathologic lesion development
distinguished diabetic Ins2Akita and normoglycemic non-Akita
B1RB2R -/- mice at 6 months of age.
This doubly-targeted Bdkrb1/Bdkrb2 stock is useful for
studying the kallikrein-kinin system, specifically the role
of bradykinin B1 receptor and bradykinin B2 receptor in
oxidative stress, mitochondrial DNA damage, apoptosis,
morphological and functional kidney changes, and other
senescence-associated phenotypes.
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