蛙心筋単一線維の興奮収縮連関に対するphenylglyoxal(PGO), dihydropyridine(dHP)及びouabainの影響 Effects of phenylglyoxal, dihydropyridine, and ouabain on the single cardiac muscle fibers of frog, Rana japonica
The present study was done to learn the mechanism of ouabain (0.1 μM) potentiation and its relation to excitation-contraction (E-C) coupling in cardiac muscle. The fibers were prepared from frog ventricle by enzymatic and mechanical disruption. Developed tensions were measured isometrically. If fibers were immersed in Ringer (22°C) containing 5 mM phenylglyoxal (PGO) for 5 min and then washed out in normal Ringer for 30 min, E-C coupling was inhibited. Ouabain cancelled the decreased tension development. DHP (200-110) gave results quite similar to PGO. 60 min after PGO-removal, rapid cooling contracture (RCC) was weakened. Ouabain-induced acceleration of RCC occurred not only under the condition of Ca- and Na-deprived Ringer but also in PGO-treated fibers. To determine the real location of Ca-transients induced by high K, fibers were fixed by replacing the bathing fluid with a solution of 1 % OsO4 and 110 mM potassium pyroantimonate. Use of energy dispersive X-ray analyzers showed that many Ca-pyroantimonate grains existed in the region near the N-line.<BR> In conclusion, both PGO and DHP inhibit E-C coupling due to binding to their respective, receptor proteins, PGO to electrometrin and DHP to DHP-protein. Also, ouabain accelerates the coupling due to binding to electrometrin (a new ouabain receptor protein).
日本薬理学雑誌 106, 82-86, 1995-09-01