Electrical activity and metabolism in cardiac tissue: An experimental and theoretical study

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Abstract
(1) Effects of the metabolic inhibitor 2,4-dinitrophenol (DNP) on electrical activity in frog atria were studied by means of the sucrose-gap technique and in tracer experiments. (2) Voltage-clamp studies of ionic membrane currents showed a suppression by DNP of peak Na inward current without marked changes in the kinetics of the Na-carrying system and an increase of steady state outward current to three to five times its normal value. In42K tracer experiments, DNP increased K resting efflux by about 10% and decreased K influx by 25 to 30%. (3) The depression of Na inward current is regarded as being caused by a partial block of Na channels and an increase of internal Na concentration after inhibition of active Na extrusion. (4) The strong rise in outward current is probably not caused by a K current since K efflux fails to show a correspondingly large change. As a possible explanation for current and flux changes, an electrogenic K pump is discussed. (5) A mathematical model of a carrier system transporting a single ion species is described. The system is designed as a direct “potential” pump. Uphill transport requires an asymmetry of the rate constants governing the cyclic formation and breakdown of carrier-ion complex. The asymmetry is brought about by an input of metabolic energy. Reduction of energy input decreases the asymmetry and induces a carrier-mediated downhill ion movement, with corresponding changes in membrane current and ion fluxes. (6) A model of electrogenic K inward transport is calculated that approximately accounts for the steady state current and the K flux changes experimentally observed after inhibition.

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