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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Circ Heart Fail. 2013 May;6(3):594–605. doi: 10.1161/CIRCHEARTFAILURE.112.000289

Figure 1. Simplified schematic of the renin-angiotensin-aldosterone system (RAAS).

Figure 1

A multitude of stressor signals induce the angiotensin gene. The prohormone angiotensinogen is cleaved by the protease Renin to the direct precursor angiotensin-I (Ang-I), and further to biologically active angiotensin-II (Ang-II). These steps can be inhibited by Renin-inhibitors or ACE-inhibitors (ACEi), respectively, but important alternative Ang-II-generating pathways exist. Alternative splicing of Ang-I and prohormones Ang-(1-12) or Ang-(1-9) by neprilysin (NEP) results in generation of Ang-(1-7). Binding of mature Ang-II to the type-1 angiotensin receptor (ATR-1) activates intracellular signaling cascades that exert adverse biological effects within the cardiovascular system such as pathological cardiac hypertrophy, vascular remodeling and renal fibrosis.