AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 283: H1092-H1098, 2002; doi:10.1152/ajpheart.00318.2001
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Vol. 283, Issue 3, H1092-H1098, September 2002

Role of protein phosphatases in hypoxic preconditioning

Yury Ladilov, Hagen Maxeiner, Christopher Wolf, Claudia Schäfer, Karsten Meuter, and H. Michael Piper

Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany

To find a protein kinase C (PKC)-independent preconditioning mechanism, hypoxic preconditioning (HP; i.e., 10-min anoxia and 10-min reoxygenation) was applied to isolated rat hearts before 60-min global ischemia. HP led to improved recovery of developed pressure and reduced end-diastolic pressure in the left ventricle during reperfusion. Protection was unaffected by the PKC inhibitor bisindolylmaleimide (BIM; 1 µmol/l). It was abolished by the inhibitor of protein phosphatases 1 and 2A cantharidin (20 or 5 µmol/l) and partially enhanced by the inhibitor of protein phosphatase 2A okadaic acid (5 nmol/l). In adult rat cardiomyocytes treated with BIM and exposed to 60-min simulated ischemia (anoxia, extracellular pH 6.4), HP led to attenuation of anoxic Na+/Ca2+ overload and of hypercontracture, which developed on reoxygenation. This protection was prevented by treatment with cantharidin but not with okadaic acid. In conclusion, HP exerts PKC-independent protection on ischemic-reperfused rat hearts and cardiomyocytes. Protein phosphatase 1 seems a mediator of this protective mechanism.

cellular calcium; heart function; ischemia; reperfusion


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