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Cardiovascular Research Advance Access originally published online on February 11, 2009
Cardiovascular Research 2009 82(1):7-8; doi:10.1093/cvr/cvp053
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

A new addition to the renin–angiotensin peptide family: proAngiotensin-12 (PA12)

Philip M. Cummins*

School of Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland

* Corresponding author. Tel: +35 31 700 7857; fax: +35 31 700 5412. Email address: phil.cummins@dcu.ie

This editorial refers to ‘Cardiac chymase converts rat proAngiotensin-12 (PA12) to angiotensin II: effects of PA12 upon cardiac haemodynamics’ by H.C.G. Prosser et al.,9 pp. 40–50, this issue.

The first 10% of the full text of this article appears below.

The renin–angiotensin system (RAS) is a pivotal physiological regulator of cardiovascular homeostasis, potently impacting hydroelectrolyte balance, arterial tone, and blood pressure as well as modulating the growth and differentiation of vascular smooth muscle cells and cardiac myocytes. In contrast, dysregulation of the RAS is intrinsically associated with cardiovascular pathologies such as hypertension, myocardial infarction, and coronary heart disease.1 The conversion of angiotensinogen to angiotensin-I (AngI, Ang1–10) by kidney-derived renin, followed by AngI conversion to AngII (Ang1–8) through angiotensin-converting enzyme type-1 (ACE1), represents the principal biochemical axis within this cascade. AngII, the main effector peptide of the RAS, subsequently exerts its broad spectrum of effects primarily through stimulation of . . . [Full Text of this Article]


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Cardiac chymase converts rat proAngiotensin-12 (PA12) to angiotensin II: effects of PA12 upon cardiac haemodynamics
Hamish C.G. Prosser, Malcolm E. Forster, A. Mark Richards, and Chris J. Pemberton
Cardiovasc Res 2009 82: 40-50. [Abstract] [Full Text] [PDF]