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NDT Advance Access originally published online on January 8, 2007
Nephrology Dialysis Transplantation 2007 22(4):992-995; doi:10.1093/ndt/gfl757
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Salt-sensitive hypertension—update on novel findings

Bernardo Rodriguez-Iturbe1 and Nosratola D. Vaziri2

1Renal Service, Hospital Universitario, Universidad del Zulia and Centro de Investigaciones Biomédicas, IVIC-Zulia, Maracaibo, Venezuela and 2The Division of Nephrology and Hypertension, University of California Irvine, Irvine California, USA

Correspondence and offprint requests to: B. Rodriguez-Iturbe, Hospital Universitario, Avenida Goajira s/n, Maracaibo, Estado Zulia, Venezuela. Email: bri@iamnet.com

Keywords: Ca exchanger; Na–K-ATPase; oxidative stress; renal angiotensin; renal inflammation; salt-retention

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



   Introduction
 
The association between a high salt intake and hardened pulse was already known 4500 years ago [1], but our understanding of the central role played by the kidneys in the sodium-driven increase in blood pressure is rooted in the studies of Guyton and co-workers [2], who postulated that restoration of sodium balance after salt intake depends on a natriuretic response, driven by a transient rise in blood pressure. In essence, the blood pressure increment serves as a physiological response directed to maintain sodium balance and extracellular volume (ECV) within normal limits. Impairment of the mechanisms responsible for the pressure-natriuresis relationship will shift the curve ‘to the right’, so that higher blood pressure levels are needed to achieve the increments in urinary sodium excretion required to maintain homeostasis and the system is thereby reset at a higher blood pressure level.

Sodium loading is almost uniformly associated with . . . [Full Text of this Article]



   How does sodium retention cause essential hypertension?
 


   Mechanisms of sustained sodium retention and salt-sensitive hypertension
 

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