Abstract
It is well known that phenylglyoxal (PGO) reacts specifically with the guanidyl moiety of arginine residue in protein and the residue occurs in the active site of many enzymes. To determine the ouabain-site responsible for ouabain potentiation, following experiments were performed using frog ventricle strips: Being driven electrically (0.1 Hz), the strips were immersed in 5 mM PGO for 10 min and then were immersed in a normal Ringer’s solution. Sixty min after the treatment with PGO, the twitch tension was inhibited markedly without affecting action potential (AP); and the potassium (60 mM)-contracture was also inhibited by PGO without the change of the magnitude of potassium-induced depolarization, whereas the caffeine (50 mM)- contracture remains unaltered. When the muscle was immersed in a Ringer’s solution containing ouabain, (1 μM) the twitch tension reduced by PGO increased to the initial tension. The potassium-contracture was also potentiated by ouabain,whereas the magnitude of potassium-induced depolarization remains unchanged. The results indicate that the excitation and contraction link in the cardiac muscles was inhibited specifically by PGO,and the inhibition was removed almost completely by ouabain.
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