Renin is an aspartyl protease that is involved in the conversion of an
giotensinogen to angitensin II and hence participates in ihs regulatio
n of blood pressure. Mice are polymorphic for the number of renin gene
s with some strains harbouring two renin genes, Ren-1(d) and Ren-2. To
study the role of renin Ren-1(d) in regulating cardiovascular homeost
asis, mice with a disrupted Ren-1(d) gene were created. Analyses of ki
dney renin mRNA expression in Ren-1(d-/-)/Ren-(2+/+) mice demonstrated
that only Ren-2 transcripts were present. Mean arterial blood pressur
es of Ren-1(d+/+)/Ren-2(+/+), Ren-1d(+/-)/Ren-2(+/+) and Ren-1(d-/-)/R
en-2(+/+) mice showed no significant differences. These observations d
emonstrate that the Ren-1(d) gene product is not essential for normal
blood pressure maintenance under normal physiological conditions.