Cellular and Molecular Life Sciences CMLS

, Volume 61, Issue 21, pp 2720–2727

What’s new in the renin-angiotensin system?

Novel angiotensin peptides
Multi-author Review

DOI: 10.1007/s00018-004-4243-4

Cite this article as:
Ferrario, C.M. & Chappell, M.C. CMLS, Cell. Mol. Life Sci. (2004) 61: 2720. doi:10.1007/s00018-004-4243-4


Virtually all existing evidence on the function of angiotensin II (Ang II) in the regulation of tissue homeostasis and blood pressure regulation bears on the more restricted question of what other mechanisms or systems may amplify or inhibit the actions of this important peptide. Whereas there is evidence that Ang II may potentiate the effects of catecholamines, various cytokines and also growth factors, the repertoire of substances which may inhibit the actions of Ang II is more limited and has been restricted primarily to prostacyclin, bradykinin and nitric oxide. Advances in receptor pharmacology and introduction of selective antagonists to two of the receptor subtypes at which Ang II binds permitted a more critical examination of the functions of the renin angiotensin system in physiological and pathophysiological conditions, as well as uncovering the previously unsuspected possibility that within the biochemical pathways leading to the formation of the peptide the renin angiotensin system could process either its immediate precursor (angiotensin I) or the actual Ang II peptide into an alternative form, angiotensin-(1–7) [Ang-(1–7)], the function of which was to antagonize the effects of Ang II. We review here the biological actions of Ang-(1–7) and discuss how this discovery may change altogether the perception of how the renin angiotensin system functions in the regulation of tissue perfusion pressure and the regulation of salt and water metabolism.

Key words.

Angiotensin peptides ACE2 blood pressure cardiac hypertrophy heart failure hypertension renal function renin angiotensin system 

Copyright information

© Birkhäuser Verlag, Basel 2004

Authors and Affiliations

  1. 1.The Hypertension and Vascular Disease CenterWake Forest University School of MedicineWinston SalemUSA

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