Dahl SS rat
The Dahl salt sensitive (Dahl SS) rat is an established model of salt
sensitive hypertension. High salt caused an increase in message for
complement regulator CD59 in aortic tissue, with minimal change in the
mouse-specific complement regulator Crry that controls the C3
convertase. Soluble complement receptor 1 (sCR1) is a soluble form of
endogenous CR1 with demonstrated ability to inhibit complement
activation at the C3 and C5 convertase levels of the complement pathway.
Whilst application of sCR1 effectively inhibited total hemolytic
complement activity as well as C3a generation in the Dahl SS rat model,
sCR1 did not alter development of hypertension or albuminuria. This data
indicate that complement activation is not critical for development of
the salt-sensitive phenotype in Dahl rats or that the used approach to
inhibit complement activation is not useful in this model of
hypertension (Regal et al., 2018).