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Antiadrenergic effects of adenosine on His-Purkinje automaticity. Evidence for accentuated antagonism

B B Lerman1, R C Wesley, J P DiMarco

  • 1Department of Medicine, University of Virginia Medical Center, Charlottesville 22908.

The Journal of Clinical Investigation
|December 1, 1988
PubMed

Insights

Adenosine primarily counteracts the effects of adrenaline on the human His-Purkinje system (HPS). This antiadrenergic action, blocked by aminophylline, may help balance oxygen supply and demand during stress.

Area of Science:

  • Cardiovascular Physiology
  • Electrophysiology
  • Pharmacology

Background:

  • The His-Purkinje system (HPS) is crucial for cardiac impulse conduction.
  • Adenosine's role in modulating the HPS, particularly its interaction with adrenergic agents, requires further elucidation.
  • Complete atrioventricular (AV) block presents unique challenges in understanding cardiac conduction pathways.

Purpose of the Study:

  • To investigate the antiadrenergic effects of adenosine on the human His-Purkinje system (HPS).
  • To determine the mechanism by which adenosine antagonizes catecholamine effects in the HPS.
  • To explore the potential clinical implications of adenosine's interaction with the HPS in conditions like AV block.

Main Methods:

  • Studied adenosine's effects on HPS cycle length in nine patients with complete AV block.
  • Administered isoproterenol and adenosine, then assessed HPS cycle length.
  • Utilized aminophylline, an adenosine antagonist, to observe its effect on adenosine's antiadrenergic action.
  • Examined isolated guinea pig hearts with induced AV block, using isoproterenol and an adenosine antagonist (1,3-dipropyl-8-phenyl-xanthine).

Main Results:

  • Adenosine minimally affected control HPS cycle length but significantly increased it when combined with isoproterenol (906 ms to 1,449 ms).
  • Aminophylline completely abolished adenosine's antiadrenergic effect on the HPS.
  • In guinea pig models, adenosine antagonists enhanced isoproterenol-induced decreases in HPS rate, suggesting adenosine's counter-regulatory role.

Conclusions:

  • Adenosine exerts primarily antiadrenergic effects on the human HPS, consistent with accentuated antagonism.
  • Adenosine's action may represent a counterregulatory metabolic response to improve oxygen supply-demand balance during sympathetic activation.
  • Imbalances in this adenosine-catecholamine feedback system could contribute to catecholamine-mediated ventricular arrhythmias during ischemia or stress.

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