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Cardiac responses and binding sites for endothelin in normal and cardiomyopathic hamsters

G T Bolger1, R Berry, F Liard

  • 1Department of Pharmacology, Bio-Mega Inc., Laval, Quebec, Canada.

Insights

Endothelin-1 impacts heart function differently in dystrophic hamsters compared to normal ones, showing reduced positive inotropic effects in the atrium. Binding of endothelin-1 to tissue membranes remained similar across both hamster strains.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology
  • Animal Models of Disease

Background:

  • Endothelin-1 (ET-1) is a potent vasoconstrictor peptide with diverse physiological roles.
  • Dystrophic hamster strains, like CHF 147, exhibit cardiac pathologies mimicking human cardiomyopathies.
  • Understanding ET-1's role in disease is crucial for developing targeted therapies.

Purpose of the Study:

  • To compare the functional effects of endothelin-1 on cardiac tissues in dystrophic hamsters (CHF 147) versus age-matched controls (CHF 148).
  • To investigate the binding characteristics of endothelin-1 in various tissues of both hamster strains.

Main Methods:

  • Isolated spontaneously beating atria and field-stimulated right ventricular strips were used to assess inotropic and chronotropic responses to endothelin-1.
  • Radioligand binding assays with [125I]endothelin-1 were performed on membrane preparations from atrium, ventricle, lung, kidney, and brain.

Main Results:

  • Endothelin-1 induced dose-dependent positive inotropic and chronotropic effects in atria of both CHF 148 and CHF 147.
  • A significantly less positive inotropic effect of endothelin-1 was observed in CHF 147 atria compared to CHF 148.
  • Ventricular strips from CHF 148 showed greater force than CHF 147; endothelin-1 decreased tension in both, with no strain-specific difference.
  • [125I]Endothelin-1 binding was high-affinity and irreversible in all tested tissues from both strains, with no significant differences between CHF 148 and CHF 147.

Conclusions:

  • Dystrophic hamster atria exhibit a diminished positive inotropic response to endothelin-1, suggesting altered signaling pathways in cardiomyopathy.
  • Despite functional differences in atrial contractility, endothelin-1 receptor binding appears preserved in dystrophic hearts and other tissues.

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