| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 2006;48:370.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Pediatric Surgery, Erasmus MC, Rotterdam, The Netherlands.
Correspondence to Abraham P. Provoost, Department of Pediatric Surgery, Erasmus MC, Room Wk 207, PO Box 2040, 3000 CA, Rotterdam, The Netherlands. E-mail a.provoost@erasmusmc.nl
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
For more than a century, the reninangiotensin system (RAS) has been recognized as an important part of the physiological system that regulates sodium and water homeostasis, renal function, and systemic blood pressure. The RAS consists of an enzyme/substrate cascade generating angiotensin II (Ang II). Initially the RAS was considered an endocrine system. By activating cellular receptors, circulating Ang II influences blood pressure and electrolyte balance through its effects on vascular tone, aldosterone secretion, renal sodium handling, and water intake. Nowadays, Ang II is thought to also act as a paracrine factor. Various tissues can generate Ang II, although not all RAS components are locally synthesized. Despite recently detected roles of other RAS components, such as prorenin, (pro)renin receptors, angiotensin IV, and angiotensin 1 to 7, the octapeptide Ang II is still considered the main actor of both the endocrine and paracrine RAS.
Circulating and tissue concentrations of Ang II may vary markedly. For the kidney, a model has been designed to describe the kinetics of Ang II production, distribution, and disposal.1 The model distinguishes between endocrine Ang II mainly acting in the glomerular tissue regions, whereas peritubular tissue regions are exposed to Ang II generated by the conversion of intrarenally produced angiotensin I. The model explains why the kidney is responsive to low levels of endocrine Ang II, despite its high paracrine Ang II content.
Ultimately, Ang II has its biological effects by activating signaling pathways through specific receptors. Various cellular Ang II receptors subtypes have been distinguished, with the
Related Article:
Hypertension 2006 48: 453-459.
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |