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

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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).
社団法人日本薬理学会の論文
1995-09-01