title: Does the protein kinase C pathway modulate sarcolemma damage and the release of cytosolic proteins in the rat heart?
abstract: 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 [Ca2+]o of the initial Ca(2+)-depletion phase. 2. When [Ca2+]i was raised by perfusion with caffeine or under N2, 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 Cao(2+)-depletion of the Ca(2+)-paradox. 3. The PKC inhibitor, 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine, (2 x 10(-6) M) inhibited both the Ca(2+)-paradox and caffeine-induced release of CK. 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.
authors.affiliation: Department of Environmental and Evolutionary Biology, University of Liverpool, U.K.
authors.forename: S
authors.initials: S
authors.lastname: Daniels
authors.forename: C J
authors.initials: CJ
authors.lastname: Duncan
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D000818:Animals; D002110:Caffeine / Q000037:antagonists & inhibitors; D002118:Calcium / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D007546:Isoquinolines / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism*; D010879:Piperazines / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012508:Sarcolemma / Q000473:pathology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D007546:Isoquinolines; D010879:Piperazines; D011506:Proteins; D002110:Caffeine; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium