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Endothelin-1 (ET) is a potent vasoconstrictor and promitogenic peptide produced ubiquitously by the vas- cular 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 fail- ure (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 activation of this system, with increased synthesis and subsequent overflow into plasma. The biology of the ET system, however, is more intricate due to the presence of endothelial ETB receptors that are capable of clearing circulating ET from plasma (5). Thus, the increase in circulating ET could result from increased production, reduced clearance, or a combination of both. Since the lungs display the highest ET and ECE content and are recognized as the major site for circulating ET clearance, they may occupy a central role in the modulation of plasma ET. The observation that ET levels correlate especially well with the severity of pulmonary hypertension associated with CHF lends support to this hypothesis. These observations therefore raise the possibility that increased plasma ET levels could reflect the severity of pulmonary vascular endothelial dysfunction associated with CHF. 1. Evidence for increased pulmonary ET production in

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