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Mechanisms of endothelin-1-induced decrease in contractility in adult mouse ventricular myocytes.

K Nishimaru1, Y Miura, M Endoh

  • 1Department of Cardiovascular Pharmacology, Yamagata University School of Medicine, Yamagata, Japan.

British Journal of Pharmacology
|July 21, 2007
PubMed
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Endothelin-1 (ET-1) causes negative inotropy in mouse hearts by reducing calcium transients and myofilament sensitivity. This involves increased calcium extrusion via the Na+/Ca2+ exchanger, impacting cardiac contractility.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Cardiology
  • Cellular Mechanisms of Cardiac Function

Background:

  • Endothelin-1 (ET-1) is a potent vasoconstrictor implicated in cardiovascular disease.
  • While ET-1 enhances contractility in most mammals, it paradoxically reduces it in mice.

Purpose of the Study:

  • To investigate the cellular mechanisms behind ET-1's negative inotropic effect in adult mouse ventricular myocytes.
  • To elucidate the role of calcium handling and myofilament sensitivity in ET-1-induced cardiac dysfunction.

Main Methods:

  • Simultaneous recording of cell shortening and calcium transients in isolated mouse ventricular myocytes.
  • Utilized the calcium-sensitive dye indo-1 for accurate measurements.
  • Employed the Na+/Ca2+ exchange inhibitor SEA0400 to assess exchanger involvement.

Related Experiment Videos

Main Results:

  • ET-1 decreased myocyte cell shortening and calcium transients in a dose-dependent manner.
  • ET-1 reduced myofilament calcium sensitivity, indicated by a rightward shift in the calcium transient/cell-shortening relationship.
  • The Na+/Ca2+ exchanger inhibitor SEA0400 attenuated ET-1's effects on calcium transients and cell shortening.

Conclusions:

  • ET-1 induces negative inotropy in mouse ventricular myocytes via reduced calcium transients and myofilament calcium sensitivity.
  • Increased calcium extrusion by the Na+/Ca2+ exchanger is a key mechanism underlying ET-1's effects.
  • Retarded cell shortening may contribute to the observed decrease in myofilament calcium sensitivity.