| Species |
M. musculus |
| Official Name |
B6.129S7-Bdkrb2tm1Jfh/JSmi |
| Common Name |
B6.129S7-Bdkrb2tm1Jfh/JSmi |
| Description |
Mice homozygous for the Bdkrb2 targeted mutation are viable
and fertile and display no major defects. Homozygous mutant
tissue from the ileum, uterus, and superior cervical ganglia
all failed to respond to pharmacological doses of
bradykinin. This finding supports the existance of only one
type of B2 receptor. B2 deficient mice also display a
greater hypertensive response to chronic high sodium intake
compared to controls. These mice may be used to study the
role of the B2 receptor in hypertension, inflammation, the
cardiovascular system, renal function and reproduction.
|
| Development Status |
Breeding complete |
| Creation Method |
knockout |
| Background |
C57BL/6J |
| Breeding Generations |
6 |
| Phenotype Description |
Mice that are homozygous for the targeted disruption of the
gene encoding the B2 bradykinin receptor have been
generated. The gene disruption results in a deletion of the
entire coding sequence for the B2 receptor. The disruption
of the B2 receptor gene has been confirmed by genetic,
biochemical, and pharmacological analyses. Mice that are
homozygous for the disruption of the B2 receptor gene are
fertile and indistinguishable from their littermates by
visual inspection. Bradykinin fails to produce responses in
pharmacological preparations from ileum, uterus, and the
superior cervical ganglia from these mice. Therefore,
expression of a single gene appears to be responsible for
conferring responsiveness to bradykinin in these tissues.
|