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Heart failure and endothelin receptor antagonists

T Miyauchi1, K Goto

  • 1Department of Internal Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.

Trends in Pharmacological Sciences
|June 4, 1999
PubMed

Insights

Endothelin-1 is elevated in heart failure. Blocking endothelin receptors with an antagonist improves survival and cardiac function in animal models, suggesting a new therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Pharmacology
  • Heart Failure Research

Background:

  • Endothelin-1 (ET-1) is produced by cardiac myocytes and vascular endothelial cells.
  • ET-1 increases cardiac and vascular smooth muscle contractility and causes myocardial hypertrophy and cellular injury.
  • ET-1 production is significantly elevated in the failing heart.

Purpose of the Study:

  • To evaluate the therapeutic potential of endothelin receptor antagonists (ERAs) for heart failure treatment.
  • To investigate the long-term effects of ERAs on survival and cardiac function in heart failure models.

Main Methods:

  • Review of evidence on endothelin receptor antagonist efficacy.
  • Analysis of animal studies (rat, hamster) with chronic heart failure treated with ERAs.

Main Results:

  • Long-term ERA treatment significantly improved survival rates in animal models of chronic heart failure.
  • Beneficial effects included amelioration of left ventricular dysfunction.
  • The myocardial endothelin system is implicated in heart failure pathophysiology.

Conclusions:

  • Endothelin receptor antagonists show promise as a novel therapeutic strategy for heart failure.
  • Targeting the myocardial endothelin system offers a new avenue for heart failure intervention.

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