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Arrhythmogenic action of endothelin-1(1-31) through conversion to endothelin-1(1-21)

An-Jing Ren1, Xin Yuan, Li Lin

  • 1Department of Physiology, Basic Medical College, Second Military Medical University, Shanghai, China.

Experimental Biology and Medicine (Maywood, N.J.)
|June 3, 2006
PubMed

Insights

Endothelin (ET)-1(1-31) causes heart arrhythmia in rats, likely by converting to ET-1(1-21). Blocking ET(A) receptors with BQ123 reduced this effect, suggesting a role for ET(A) receptors in ET-1(1-31)-induced arrhythmia.

Area of Science:

  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Endothelin (ET)-1(1-21) is implicated in acute ischemic arrhythmia pathogenesis.
  • The role of the precursor peptide ET-1(1-31) in inducing cardiac arrhythmia is not well understood.

Purpose of the Study:

  • To investigate the arrhythmogenic potential of ET-1(1-31) in isolated perfused rat hearts.
  • To explore the underlying mechanisms, including the involvement of ET(A) receptors and the conversion to ET-1(1-21).

Main Methods:

  • Isolated rat hearts were perfused using the Langendorff technique.
  • Hearts were exposed to varying concentrations of ET-1(1-31) with or without antagonists (BQ123) or enzyme inhibitors (phosphoramidon).
  • Arrhythmia, heart rate, coronary flow, and cardiac function were monitored and analyzed.

Main Results:

  • Perfusion with 1 nM ET-1(1-31) significantly increased ventricular ectopic beats (VEBs) and ventricular tachycardia (VT).
  • Pretreatment with the ET(A) receptor antagonist BQ123 markedly attenuated the ET-1(1-31)-induced arrhythmia.
  • The neutral endopeptidase inhibitor phosphoramidon partially reduced the arrhythmogenic effects, suggesting conversion to ET-1(1-21) plays a role.

Conclusions:

  • ET-1(1-31) induces cardiac arrhythmia in isolated perfused rat hearts.
  • This arrhythmogenic action is partly mediated by ET(A) receptors.
  • The effect is largely attributed to the conversion of ET-1(1-31) to the more potent ET-1(1-21).

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