Abstract
Experimental and clinical studies have highlighted the importance of the local renin-angiotensin system (RAS) as a pathogenetic factor in various tissues, including the kidney, heart, and eye.1 These studies have indicated that blockade of the RAS is an important therapeutic strategy in reducing cardiovascular and renal disease. However, the therapeutic response achieved with current blockers of the RAS—angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)—although efficacious, is limited. This may be partly because of the reactive rise in renin that these agents induce with the resultant increase in angiotensin peptides. Other, more effective strategies to block the RAS have, therefore, been sought. Angiotensin II, the major effector molecule of this system, is synthesized in a multistep process in which angiotensinogen is cleaved by the aspartic peptidase, renin, produced mainly in the juxtaglomerular cells of the kidney, to give to rise to angiotensin I. …
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