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Desipramine prevents cardiac gap junction uncoupling.

Joanna Jozwiak1, Anna Dietze, Rajiv Grover

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Desipramine prevents cardiac gap junction uncoupling and reduces arrhythmogenic dispersion during ischemia/reperfusion. This antidepressant shows potential in managing cardiac arrhythmias by stabilizing gap junctions.

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Cardiac gap junction uncoupling is a key mechanism in ischemia/reperfusion-induced arrhythmias.
  • Antiarrhythmic peptide AAP10 prevents acidosis-induced uncoupling and dispersion.
  • Desipramine, a tricyclic antidepressant, may share similar effects with AAP10 based on structural studies.

Purpose of the Study:

  • To investigate the potential of desipramine in preventing cardiac gap junction uncoupling and associated arrhythmogenic mechanisms.
  • To compare the effects of desipramine with AAP10 in cardiac models.

Main Methods:

  • Radioligand binding assays using (14)C-AAP10 and desipramine to assess binding affinity.
  • Measurement of gap junction currents in isolated human atrial cardiomyocytes under normal and acidotic conditions with desipramine.
  • Electrophysiological mapping and analysis of connexin43 (Cx43) expression, phosphorylation, and localization in isolated rabbit hearts undergoing ischemia with desipramine.

Main Results:

  • Desipramine displaced (14)C-AAP10 binding to cardiac membranes, indicating interaction.
  • Desipramine significantly reversed acidosis-induced reduction in gap junction conductance in human cardiomyocytes.
  • Desipramine prevented ischemia-induced increases in dispersion, Cx43 loss, and dephosphorylation in rabbit hearts.

Conclusions:

  • Desipramine effectively prevents the uncoupling of cardiac gap junctions.
  • Desipramine mitigates ischemia-related increases in cardiac electrical dispersion.
  • The findings suggest desipramine has potential antiarrhythmic properties by targeting cardiac gap junctions.