Abstract
Evidence is summarized which indicates that the positive inotropic effect (PIE) of theophylline, which is similar to that observed with β-adrenoceptor stimulating agents, in mammalian cardiac muscle is mainly due to an increase in slow inward current, Isi . The increase in Isi and, hence, in force of contraction conceivably results from an inhibition of phosphodiesterase (PDE) activity with a subsequent increase in myocardial cAMP levels. The increase in cAMP levels is probably also responsible for the relaxant effects of theophylline in smooth muscle. Finally it is discussed that the PIE of theophylline in the heart is unlikely to result from an adenosine-antagonistic action because adenosine produces a negative inotropic effect only in atria, whereas in ventricular cardiac muscle it even increases the force of contraction.
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