Skip Navigation


NDT Advance Access originally published online on June 7, 2007
Nephrology Dialysis Transplantation 2007 22(9):2426-2429; doi:10.1093/ndt/gfm321
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/9/2426    most recent
gfm321v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Burnier, M.
Right arrow Articles by Wang, Q.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Burnier, M.
Right arrow Articles by Wang, Q.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

High salt intake: a cause of blood pressure-independent left ventricular hypertrophy?

Michel Burnier, Olivier Phan and Qing Wang

Division of Nephrology, Department of Medicine and University of Lausanne, Lausanne, Switzerland

Correspondence and offprint requests to: M. Burnier, Division of Nephrology and Hypertension Consultation, Centre Hospitalier Universitaire Vaudois, Rue du Bugnon 17 CH-1011 Lausanne, Switzerland. Email: michel.burnier@chuv.ch

Keywords: blood pressure; cardiac hypertrophy; potassium; sodium

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



   Introduction
 
Left ventricular hypertrophy (LVH) is a frequent and well-recognized consequence of a chronically elevated blood pressure (BP). Several studies have demonstrated that LVH is an independent cardiovascular risk factor, associated with an increased likelihood to develop cardiovascular complications such as congestive heart failure, sudden cardiac death, coronary heart disease and stroke [1,2]. Conversely, an aggressive treatment of hypertension can prevent and reverse LVH and reduce the incidence of cardiovascular events [3,4].

Non-haemodynamic factors leading to LVH
If BP is definitively the major trigger for the development of cardiac hypertrophy in hypertension, left ventricular mass may be affected by several other non-haemodynamic factors which may also play an important role in the pathophysiology of LVH, as listed in Table 1. Factors such as gender, age, race, obesity, alcohol consumption, catecholamines, ANP, aldosterone and angiotensin II and genetic factors (polymorphism of ACE) have all been considered as BP-independent . . . [Full Text of this Article]

Does sodium have a role in the development of LVH?
What is the normal BP in mice with cardiac hypertrophy?


   Conclusions
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?