| Summary: | Christoph Schindler1, Peter Bramlage1, Wilhelm Kirch1, Carlos M Ferrario21Institute of Clinical Pharmacology, Medical Faculty, Technical University of Dresden, Dresden, Germany; 2Hypertension and Vascular Disease Center, Wake Forest University, School of Medicine, Winston-Salem, NC, USAAbstract: The renin-angiotensin-system (RAS) is a cascade of enzymatic reactions resulting ultimately in the formation of angiotensin II. Recent research has expanded the knowledge about the RAS by adding new components to the pathways: angiotensin-(1–5) [Ang-1–5], angiotensin-(1–7) [Ang-(1–7)], angiotensin-(1–9) [Ang-(1–9)], an ACE homologous enzyme, ACE2, and the G-protein-coupled receptor mas as a molecular receptor for Ang-(1–7). Although previous studies provided some conflicting evidence about the relevance of Ang-(1–7) in the regulation of vascular and renal function, data now demonstrate that Ang-(1–7) contributes to the cardiovascular effects of ACE-inhibitors (ACE-I) and AT1-receptor-blockers (ARBs) both in experimental conditions and in humans. This review summarizes and critically discusses the currently available experimental and clinical study evidence for the role of Ang-(1–7) as a vasodilator and anti-trophic peptide in cardiovascular drug therapy. In addition, the potential therapeutic impact of currently available RAS blocking agents (ACE-I and ARBs) and new agents still under development (renin-inhibitors) on the RAS-effector peptides is highlighted.Keywords: renin-angiotensin-system, cardiovascular drug therapy, Angiotensin-(1–7)
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