caa a22 4500 477119719 CHVBK 20180405111633.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF00240042 doi (NATIONALLICENCE)springer-10.1007/BF00240042 Signal transduction in myocardial ischaemia and reperfusion [Elektronische Daten] [A. Lochner, E. Tromp, R. Mouton] Recent studies in the non-ischaemic myocardium indicated that drugs stimulating cAMP formation inhibit α1-mediated inositol phosphate generation, while α1-adrenergic stimulation lowered tissue CAMP levels, implicating cross-talk between α1,- and β-adrenergic signalling pathways in normal physiological conditions. Massive amounts of endogenous catecholamines, predominantly noradrenaline, are released during myocardial ischaemia and reperfusion, causing stimulation of both α1- and β-adrenergic receptors which, in turn, may contribute to intracellular Ca2+ overload and subsequent cell damage. Since no information is available regarding cross-talk in pathophysiological conditions, the aim of this study was to evaluate the interactions between α1- and β-adrenergic signalling pathways during different periods of ischaemia and reperfusion. Isolated rat hearts were perfused retrogradely for 30 min before being subjected to (i) 5-25 min global ischaemia and (ii) 1-5 min of reperfusion after 20 min global ischaemia. Drugs (prazosin, 10−7 M; propranolol, 10−6 M; phenylephrine 3 × 10−5 M; isoproterenol 10−9 M) were added 10 min before the onset of ischaemia and were present during reperfusion. Increasing periods of ischaemia caused an immediate rise and progressive lowering in tissue cAMP and Ins(1,4,5)P3 levels respectively. In contrast, reperfusion caused an elevation in Ins(1,4,5)P3 levels and reduced cAMP. Prazosin elevated cAMP levels during both ischaemia and reperfusion, while propranolol had no effects on tissue Ins(1,4,5)P3−. The activity of the α1-adrenergic signal transduction pathway appears to have an inhibitory effect on the activity of the β-adrenergic system during ischaemia and reperfusion. Kluwer Academic Publishers, 1996 signal transduction nationallicence adrenergic receptors nationallicence ischaemic myocardium nationallicence ischaemia-reperfusion injury nationallicence Lochner A. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut Tromp E. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut Mouton R. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut Molecular and Cellular Biochemistry Kluwer Academic Publishers; http://www.wkap.nl 160-161/1(1996-03-01), 129-136 0300-8177 160-161:1<129 1996 160-161 11010 https://doi.org/10.1007/BF00240042 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00240042 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Lochner A. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut NATIONALLICENCE 700 1- Tromp E. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut NATIONALLICENCE 700 1- Mouton R. Department of Medical Physiology and Biochemistry, University of Stellenbosch Faculty of Medicine; MRC Programme for Experimental Biology, 7505, Tygerberg, Republic of South Africa aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Kluwer Academic Publishers; http://www.wkap.nl 160-161/1(1996-03-01), 129-136 0300-8177 160-161:1<129 1996 160-161 11010 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer