Phosphorylation of phospholamban and troponin I in the ischemic and reperfused heart: attenuation and restoration of isoprenaline responsiveness.
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| Abstract |
Acute myocardial ischemia maintained for 30 and 60 min with subsequent reperfusion did not induced alterations in the cyclic AMP-mediated phosphorylation capacity of phospholamban and troponin I. Inotropic stimulation of the normal heart with 0.1/uM isoprenaline for 2 min resulted in a simultaneous P-incorporation into phospholamban and troponin I to 44.4 +/- 7.5 pmoles P/mg protein and 42.4 +/- 2.9 pmoles P/mg protein, respectively, assayed by a standardized back-phosphorylation procedure. The adrenergic responsiveness, however, was markedly reduced in the time course of ischemia. After an ischemic period of 60 min the adrenergic-stimulated phosphorylation of phospholamban was diminished to 41 per cent of the control value, whereas the increase of troponin I phosphorylation was completely lost. This differential effect can be discussed in terms of the existence of cytosolic compartments for cA, possessing different lability to ischemic injury of cardiac cells. After post-ischemic reperfusion the isoprenaline responsiveness of the phosphorylation of phospholamban and troponin I was found to be normal demonstrating a reversibility at the level of two important regulator proteins, if the transient ischemia do not exceed 60 min period.
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| Authors | S Bartel, P Karczewski, E G Krause |
| Journal | Biomedica biochimica acta (Biomed Biochim Acta) Vol. 48 Issue 2-3 Pg. S108-13 ( 1989) ISSN: 0232-766X [Print] Germany |
| PMID | 2525030 (Publication Type: Journal Article) |
| Chemical References |
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