Abstract
1. 1. The release of creatine kinase (CK) in the Langendorff-perfused rat heart during the Ca 2+-paradox, was critically dependent on the duration and [Ca 2+] o of the initial Ca 2+ -depletion phase. 2. 2. When [Ca 2+] i was raised by perfusion with caffeine or under N 2, activation of the protein kinase C pathway (PKC) produced a small but significant release of CK. PKC stimulation is therefore able to substitute for the Ca 2+ o-depletion of the Ca 2+-paradox. 3. 3. The PKC inhibitor, 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine, (2 × 10 −6 M) inhibited both the Ca 2+-paradox and caffeine-induced release of CK. 4. 4. It is concluded that the PKC pathway has a regulatory role for the damage system of the sarcolemma that is responsible for the release of cytosolic proteins.
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