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NDT Advance Access originally published online on September 8, 2006
Nephrology Dialysis Transplantation 2006 21(11):3048-3051; doi:10.1093/ndt/gfl411
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Dogmas and surprises about the renin–angiotensin system and sodium reabsorption*

Branko Braam and Hein A. Koomans

Deptartment of Nephrology and Hypertension, University Medical Center Utrecht, The Netherlands

Correspondence and offprint requests to: Branko Braam, MD, PhD, Department of Nephrology and Hypertension – F03.223, University Medical Center Utrecht, The Netherlands. Email: bbraam@gmail.com

Keywords: glomerulotubular balance; proximal tubule; RAS; sodium handling; tubuloglomerular feedback

The first 150 words of the full text of this article appear below.



   Introduction
 
After many years of studies on the renin–angiotensin system (RAS), one of the central concepts is that the RAS forms an effective defence mechanism against low-sodium states and hypotension. Low-perfusion pressure sensed by the afferent arteriole, low-distal delivery sensed by the macula densa and low blood pressure sensed by the sympathetic nervous system increase renin release, leading to angiotensin generation and sodium retention, vasoconstriction and restoration of blood pressure. About 15 years ago, the first reports appeared indicating angiotensin concentrations in the proximal tubule of higher magnitude than in the plasma [1,2]. Attempts to relate intraluminal angiotensin II (Ang II) concentrations to the functionality ascribed to the RAS were not very successful: the intratubular system did not seem to be adapting synchronously with the systemic RAS. What is the matter here? Is there a local RAS that acts independently from the systemic RAS? What would be . . . [Full Text of this Article]



   The classical view: the RAS is a sodium-retaining mechanism
 


   The proximal tubular angiotensin system; what do we know?
 


   The surprise: sodium loading in rat increases intratubular Ang II levels and is associated with maintained Ang II-dependency of proximal tubular reabsorption
 


   What could be the physiological implication of a local and a systemic RAS with opposing functions?
 


   What implications could be envisioned of the intratubular Ang II system for clinical syndromes?
 


   Conclusions
 

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