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- W1968085461 abstract "Abstract Catecholamines, methylxanthines, and histamine, agents which increase the cyclic AMP level, are well known to increase the slow inward current ( I si ) in heart muscle. These agents can restore excitability to partially depolarized heart cells (fast Na + channels voltage inactivated) in the form of slow action potentials, whose electrogenesis is due to a regenerative increase in I si . In order to further clarify the relationship between cyclic AMP and the myocardial slow inward current, cyclic AMP was applied intracellularly in an attempt to restore slow action potentials in cardiac Purkinje fibers. The Purkinje fibers were taken from canine hearts, shortened to a length of 2 to 3 mm, and superfused at 10 ml/min with Krebs-Henseleit solution. Superfusion with an elevated K + (20 m m ) solution depolarized the fibers to about −40 mV and rendered the preparations inexcitable. Intracellular microiontophoresis of cyclic AMP (0.2 to 12 μC) restored slow action potentials in 25 out of 46 cells so tested. The induced slow action potentials persisted for a transient period of 1 to 5 min following the injection. In a separate series of experiments, theophylline (0.5 m m ) was used to induce slow action potentials. Cyclic AMP injection increased the maximal upstroke velocity ( + v max ) and overshoot of these ongoing slow action potentials. The effects obtained increased with the amount of cyclic AMP injected. A similar potentiation of the slow action potential was found in ventricular muscle (guinea-pig papillary muscles). The results indicate that cyclic AMP, applied intracellularly, can mimic the well-known restorative action of catecholamines and methylxanthines in partially depolarized heart muscle. This confirms a relationship between cyclic AMP and the net slow inward current." @default.
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- W1968085461 date "1981-01-01" @default.
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- W1968085461 title "Induction of slow action potentials by microiontophoresis of cyclic AMP into heart cells" @default.
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- W1968085461 doi "https://doi.org/10.1016/0022-2828(81)90228-5" @default.
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