The activity of a local cardiac renin-angiotensin system (RAS) has long bee
n suspected in the promotion of cardiac pathologies including hypertrophy,
ischemia, and infarction. All of the components of the RAS cascade have bee
n demonstrated to be synthesized within the heart with the possible excepti
on of the first enzyme in the cascade, renin. In the current study, we prov
ide direct evidence that circulating renin can contribute to cardiac-specif
ic synthesis of angiotensin peptides. Furthermore, we demonstrate this effe
ct is independent of blood pressure and that in animals of comparable blood
pressure, elevated circulating renin significantly enhances cardiac fibros
is. These results may serve to explain some of the cardiac pathologies asso
ciated with the RAS.