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Phosphatase inhibitor cantharidin blocks adenosine A(1) receptor anti-adrenergic effect in rat cardiac myocytes

P Narayan1, R M Mentzer, R D Lasley

  • 1Department of Surgery, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA. pnaraya@pop.uky.edu

American Journal of Physiology. Heart and Circulatory Physiology
|January 25, 2000
PubMed

Insights

Protein phosphatases partially mediate the anti-adrenergic effects of adenosine A(1) receptor activation in heart cells. Cantharidin, a protein phosphatase inhibitor, blocked these effects, suggesting a key role for phosphatases.

Area of Science:

  • Cardiology
  • Molecular Pharmacology
  • Cell Physiology

Background:

  • Adenosine A(1) receptors modulate cardiac function.
  • Anti-adrenergic effects in the heart are complex and involve various signaling pathways.

Purpose of the Study:

  • To investigate the role of protein phosphatases in the anti-adrenergic effects of adenosine A(1) receptor stimulation.
  • To determine if cantharidin, a protein phosphatase inhibitor, affects adenosine A(1) receptor-mediated signaling in cardiomyocytes.

Main Methods:

  • Experiments utilized electrically stimulated adult rat ventricular myocytes.
  • Measurements included intracellular calcium concentration ([Ca(2+)](i)), twitch amplitude, and cellular cAMP levels.
  • The effects of isoproterenol, CCPA (adenosine A(1) receptor agonist), and cantharidin were assessed.

Main Results:

  • Isoproterenol increased [Ca(2+)](i), contractility, and cAMP.
  • CCPA attenuated isoproterenol's effects on [Ca(2+)](i) and contractility, but not cAMP.
  • Cantharidin blocked CCPA's effects on [Ca(2+)](i) and contractility, without altering cAMP levels or isoproterenol's effects.

Conclusions:

  • Activation of protein phosphatases plays a partial role in the anti-adrenergic effects of adenosine A(1) receptor activation in ventricular myocardium.
  • These findings highlight a novel signaling mechanism involving protein phosphatases in cardiac regulation.

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