Dimethylxanthine-induced inhibition of residual fast channel in deporalized ventricular muscle

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This study was performed to elucidate the mechanism of dimethylxanthine (theophylline)induced reduction of the maximum rate of rise (Vmax) of action potentials in guinea pig papillary muscle perfused with Tyrode's solution of different K+ concentrations(2.7-13.5mM). At. relatively high [K+]o concentrations(8.1-13.5mM), the Vmax is composed of 2 components, i. e., the Vmax, fast followed by the Vmax, slow. The Vmax, fast was a measure of the residual (partly inactivated) fast channel while the Vmax, slow represents the slow channel. Theophylline depressed Vmax, fast with and increase in Vmax, slow in a concentrationdependent manner (1-4mM). The depression of Vmax, fast by this agent was remarkable in more depolarized membranes and was attributed to the negative shift of the curve relating Vmax, fast to the resting potentials along the voltage axis. A similar shift occurred in the presence of dibutyryl- cAMP(3mM). These results suggested that theophylline blocks the residual Na+ channel in depolarized ventricular muscle via an increase of cellular cAMP.
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