Circulating renin contributes to local cardiac angiotensin synthesis and promotes cardiac fibrosis independent of blood pressure, providing a mechanism for RAS-associated cardiac pathologies.
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May promote cardiac fibrosis beyond BP control in patients; leaves open clinical translation of renin-targeted strategies.
The activity of a local cardiac renin-angiotensin system (RAS) has long been suspected in the promotion of cardiac pathologies including hypertrophy, ischemia, and infarction. All of the components of the RAS cascade have been demonstrated to be synthesized within the heart with the possible exception of the first enzyme in the cascade, renin. In the current study, we provide direct evidence that circulating renin can contribute to cardiac-specific synthesis of angiotensin peptides. Furthermore, we demonstrate this effect is independent of blood pressure and that in animals of comparable blood pressure, elevated circulating renin significantly enhances cardiac fibrosis. These results may serve to explain some of the cardiac pathologies associated with the RAS.
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Prescott et al. (2000) studied this question.
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