© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Vasopressin antagonists in CHF: ready for clinical trials?
Cardiology Division, Hennepin County Medical Center, 701 Park Avenue, Minneapolis MN 55415, USA
srg_hcmc@yahoo.com
* Tel.: +1-612-347-2875; fax: +1-612-904-4224
Received 28 January 2002; accepted 28 January 2002
| The first 10% of the full text of this article appears below. |
See article by Naitoh et al. [7] (pages 51–57) in this issue.
Improving survival in congestive heart failure is currently based on blunting the effects of inappropriately increased adrenergic drive, as well as of increased circulating and tissue levels of angiotensin II and aldosterone [1–5].The sympathetic nervous system and renin–angiotensin system comprise two of the three components of the neurohumoral axis originally proposed as links to the fundamental pathophysiology of heart failure in 1984 [6]. The third component of that axis as originally postulated was arginine vasopressin (AVP). Research into the possible role of AVP in heart failure has been hampered until comparatively recently by the absence of appropriate antagonists. Now, however, highly effective antagonists of the V1a and V2 receptors for AVP are available, and at least in preliminary human studies, are safe and well tolerated. The study by
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S. S. Gottlieb The neurohormonal paradigm:have we gone too far? J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1458 - 1459. [Full Text] [PDF] |
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