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Am J Physiol Regul Integr Comp Physiol 283: R153-R160, 2002. First published February 14, 2002; doi:10.1152/ajpregu.00491.2001
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Vol. 283, Issue 1, R153-R160, July 2002

Decreased susceptibility of cardiac function to hypoxia-reoxygenation in renin-angiotensinogen transgenic rats

Kay-Dietrich Wagner1, Vanja Essmann1, Karsten Mydlak2, Manfred Wirth3, Gunnar Gmehling1, Jürgen Bohlender4, Harald M. Stauss1, Joachim Günther1, Ingolf Schimke2, and Holger Scholz1

1 Johannes Müller Institut für Physiologie and 2 Klinik für Innere Medizin I, Humboldt Universität, Charité, 3 Institute of Freshwater Ecology and Inland Fisheries, and 4 Franz Volhard Clinic at Max Delbrück Center, Humboldt University of Berlin, Berlin, and Department of Nephrology, University of Jena, Jena, Germany

We tested the hypothesis that the renin-angiotensin system (RAS) protects the contractile function of the myocardium against the damaging effect of hypoxia-reoxygenation. For this purpose, the contractility of isolated papillary muscles from wild-type (WT) rats and from rats expressing human renin and angiotensinogen as transgenes (TGR) was compared. After 15 min of hypoxia, peak force (PF) was decreased to 24 ± 5% of the normoxic values in TGR (n = 10) and to 18 ± 1% in WT rats (n = 12). PF and relaxation rates recovered completely in TGR but not in WT rats during 45 min of reoxygenation. Improved contractility of the papillary muscles from TGR during hypoxia-reoxygenation correlated with increased glutathione peroxidase activities and creatine kinase (CK)-MB and CK-BB isoenzyme levels. On the other hand, inhibition of the RAS with ramipril (1 mg/kg body wt for 3 wk) in WT animals resulted in deterioration of the contractile function of the papillary muscles during reoxygenation compared with untreated rats. These findings suggest that activation of the RAS protects contractile function of the cardiac muscle against hypoxia-reoxygenation, possibly through changes in CK isoenzymes and enhanced antioxidant capacity.

papillary muscle; free radicals; antioxidant enzymes; creatine kinase; cardiac hypertrophy


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