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Cardiovascular Research 1998 38(3):646-654; doi:10.1016/S0008-6363(98)00057-1
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

The cardiac adrenergic system in ischaemia: differential role of acidosis and energy depletion

Gregor Simonis, Rainer Marquetant, Jochen Röthele and Ruth H Strasser*

University of Heidelberg,3 Medical Center, Dept. Cardiology, Heidelberg, Germany

* Corresponding author. Tel.: +49 (6221) 56 86 77; Fax: +49 (6221) 56 81 27.

Objective: Acute myocardial ischaemia has been shown to modulate the β-adrenergic system and to activate protein kinase C. The aim of this study was to investigate if two important components of ischaemia, i.e. energy depletion or acidosis, may contribute to these changes. Methods: Isolated rat hearts were perfused either with anoxia (in the absence of oxygen) or with cyanide in the absence of glucose as models of energy depletion with a loss of high energy phosphates. Alternatively, isolated hearts were perfused with acidic modified Krebs–Henseleit solution to induce acidosis. Results: Energy depletion induced by cyanide perfusion leads to an increase of β-adrenergic receptors (81±7 vs. 50±3 fmol/mg protein, p≤0.05) comparable to the changes observed in ischaemia, yet without any change of total adenylyl cyclase activity or protein kinase C activity. Similar, yet less pronounced changes were induced by anoxic perfusion. Acidic perfusion, in contrast, promotes a translocation of protein kinase C to the plasma membranes, suggesting its rapid activation. Additionally, an increased total forskolin-stimulated activity of adenylyl cyclase (515±16 vs. 428±17 pmol/min/mg, p≤0.05) was observed. Both were comparable to the sensitization observed in early ischaemia. In acidosis, the density of β-adrenergic receptors remained unaltered. Conclusions: These data suggest that the regulation of cardiac β-adrenergic receptors is susceptible to energy depletion, but not to acidosis, whereas the intracellular enzymes both adenylyl cyclase and protein kinase C may be regulated by intracellular acidosis. This is the first differentiation of distinct components of ischaemia modulating the β-adrenergic signal transduction pathway. Both components may be operative in concert in acute myocardial ischaemia and may contribute to the regulation of these components of signal transduction observed in acute ischaemia.

KEYWORDS Acute myocardial infarction; Protein kinase C; Heart; Signal transduction; Acidosis; Adenylyl cyclase; β-adrenergic receptors; Rat


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