In addition to being the major site for release of systemic renin, the kidney has a local renin-angiotensin system that is involved in renal growth.44 ACE-I administration during pregnancy causes severe fetal renal abnormalities. The tubular epithelial cells contain ACE, and local A-II is found in proximal tubules and mesangial cells.45 The intrarenal A-II constricts afferent and efferent arterioles and directly increases Na⁺ reabsorption. Locally, A-II is also involved in renal pathologic conditions (e.g., the development of nephrosclerosis).

Evidence exists for a role for an intracardiac renin-angiotensin system in both normal and failing hearts.41,42 There is a direct expression of AGT and the A-II receptor (AT₁) in cardiomyocytes. The exact source of the renin in cardiac tissue is controversial, because levels of mRNA are low.43 The heart can also express A-I, which may be converted by intracardiac ACE to A-II.43 Probably, cardiac renin-angiotensin system activity is regulated by the amount of AGT, ACE, or renin-binding protein in the cardiomyocytes. Consequently, local A-II can regulate vascular tone, contractility, growth, and cardiac hypertrophy.