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Endothelin receptors in the failing and nonfailing human heart

K Pönicke1, M Vogelsang, M Heinroth

  • 1Institut für Pharmakologie und Toxikologie, Universität Halle-Wittenberg, Halle, Germany.

Circulation
|March 14, 1998
PubMed

Insights

The cardiac endothelin-A (ETA) receptor system is functionally unchanged in chronic heart failure (CHF) patients. This study found that ETA receptors in the human heart are important for signaling, but their responsiveness is not altered in CHF.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Pharmacology
  • Receptor Biology

Background:

  • Elevated plasma endothelin-1 (ET-1) levels are observed in patients with chronic heart failure (CHF).
  • The potential alteration of the cardiac endothelin (ET) receptor system in CHF patients requires investigation.

Purpose of the Study:

  • To investigate the functional characteristics and density of the cardiac ET-receptor system in patients with end-stage CHF compared to non-failing hearts (NFH).
  • To determine if the ET-receptor system's responsiveness is altered in the human heart during CHF.

Main Methods:

  • Assessed ET-evoked inositol phosphate (IP) formation and ET-receptor density in right atrial and left ventricular tissues.
  • Studied ET-induced inhibition of adenylyl cyclase activity in response to isoprenaline and forskolin.
  • Utilized [125I]ET-1 binding assays and measured left ventricular Gq/11 protein levels.

Main Results:

  • ET-1 concentration-dependently increased IP formation in both NFH and CHF hearts via ET(A)-receptor stimulation, with no difference in potency or efficacy.
  • ET(A)-receptor stimulation inhibited adenylyl cyclase in right atria but not left ventricles of NFH and CHF hearts, with similar potency and efficacy.
  • No significant differences were found in ET(A)-receptor density or Gq/11 protein levels between NFH and CHF hearts.

Conclusions:

  • Both ET(A) and ET(B) receptors coexist in the human heart, but only ET(A) receptors are functionally significant.
  • In the human heart, ET(A) receptors mediate IP formation in both atria and ventricles, and inhibit adenylyl cyclase in atria.
  • The functional responsiveness of the cardiac ET(A)-receptor system remains unaltered in end-stage chronic heart failure.
Abstract

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