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Cardiovascular Research 2004 64(3):381-383; doi:10.1016/j.cardiores.2004.08.015
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

The neuroendocrine-immune interface gone awry in aldosteronism

Karl T. Weber*

Division of Cardiovascular Diseases, University of Tennessee Health Science Center, 920 Madison Avenue, Third Floor, Memphis, TN 38163, USA

* Tel.: +1 901 448 5750; fax: +1 901 448 8084. Email address: KTWeber@utmem.edu

Received 16 August 2004; accepted 25 August 2004

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

See article by Lal et al. (pages 437-447) in this issue.

Congestive heart failure (CHF), a clinical syndrome with characteristic signs and symptoms, is a salt-avid state whose origins are rooted in neurohormonal activation, including the circulating renin-angiotensin-aldosterone system (RAAS). A systemic illness accompanies CHF and contributes to a progressive downhill clinical course and poor prognosis. Features include: (a) oxi/nitrosative stress in such diverse tissues as skin, skeletal muscle, heart, lymphocytes and monocytes; (b) a proinflammatory phenotype involving multiple tissues and blood and expressed as elevated levels of chemokines and such cytokines as IL-6 and TNF-{alpha}; and (c) a catabolic state with loss of lean tissue, fat and bone that eventuates in a wasting syndrome termed cardiac cachexia. The pathophysiology of CHF includes . . . [Full Text of this Article]


   1. The neuroendocrine-immune interface
 

   2. Aldosteronism and the immune system
 

   3. Aldosteronism and the Central Nervous System (CNS)
 
3.1 Hypertension
3.2 Heart failure

   4. Summary
 

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