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Cardiovascular Research 2004 63(1):5-7; doi:10.1016/j.cardiores.2004.04.007
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Increased endothelin levels in congestive heart failure: does it come from the lungs? Does it matter?

Jocelyn Dupuis*

Research Center, Montreal Heart Institute and University of Montreal, 5000 Belangar Street East, Montreal, Quebec, Canada H1T 1C8

*Corresponding author. Tel.: +1-514-376-3330; fax: +1-514-376-1355. Email address: jocelyn.dupuis@bellnet.ca

Received 30 March 2004; accepted 13 April 2004

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

See article by von Lueder et al. [14] (pages 41–50) in this issue.

Endothelin-1 (ET) is a potent vasoconstrictor and promitogenic peptide produced ubiquitously by the vascular endothelium. It is formed by cleavage of the 39-amino acid precursor big endothelin-1 (big ET) through the action of the endothelin converting enzymes (ECEs). Although it is generally accepted that ET is released constitutively in a preferentially paracrine fashion, a smaller, measurable fraction is released into the vascular lumen. Circulating ET levels are increased in various cardiovascular conditions, including congestive heart failure (CHF) [1–3], and are related to the subsequent event rate [4].

At first glance, it could be straightforwardly concluded that higher circulating ET levels reflects . . . [Full Text of this Article]


   1. Evidence for increased pulmonary ET production in CHF
 

   2. Evidence for reduced pulmonary ET clearance in CHF
 

   3. Can we discern clearance and production?
 

   4. Can we quantify the relative contribution of the lungs to plasma ET?
 

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