Modification of the β-Adrenergic Mechanisms in Myocardium by Divalent Cations

  • D. W. Corder
  • C. E. Heyliger
  • R. E. Beamish
  • N. S. Dhalla
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 46)


Irrespective of the type and nature of stressful stimulus, elevated levels of circulating catecholamines are commonly observed. A small amount of catecholamines released in acute and mild stress is considered to increase heart function beneficially by binding to the β-adrenergic receptors, activating the adenylate cyclase system and raising the intracellular concentration of calcium (1,2). In this regard it should be mentioned that β-adrenergic receptors are coupled to adenylate cyclase by guanine nucleotide binding protein, and their activation by catecholamines is associated with formation of cyclic AMP, phosphorylation of Ca2+-channels through protein kinase and subsequent increase in the entry of Ca2+ into the myocardial cell. On the other hand, an excessive amount of catecholamine released in chronic and severe stress is believed to produce cardiotoxic effects which are associated with the occurrence of an intracellular Ca2+ overload and abnormalities in the excitation-contraction coupling process (3,4,5). Although participation of the β-adrenergic receptor-adenylate cyclase mechanism in raising the intracellular concentration of calcium is obvious at initial stages, its role in later stages with prolonged exposure of the myocardium to high doses of catecholamines is not clear at present. This view is based on the fact that prolonged exposure of tissue to catecholamines has been shown to produce desensitization of adrenergic receptors (6,7,8).


Divalent Cation Adrenergic Receptor Cyclase Activity Adenylate Cyclase Activity Guanine Nucleotide Binding Protein 
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Copyright information

© Martinus Nijhoff Publishing, Boston 1985

Authors and Affiliations

  • D. W. Corder
    • 1
  • C. E. Heyliger
    • 1
  • R. E. Beamish
    • 1
  • N. S. Dhalla
    • 1
  1. 1.Experimental Cardiology Section, Department of Physiology, Faculty of MedicineUniversity of ManitobaWinnipegCanada

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