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DNP (2,4 dinitrophenol) in concentrations of 2–5 x 10–5 m produced a shortened action potential duration (APd), a decrease in the magnitude of the AP, and a depression of contractility in the isolated perfused frog heart and the mouse atrium. There was a close correlation between the shortened APd and depression of contractility. The membrane resting potential was unchanged even during the period of cardiac arrest. The following mechanisms are postulated to explain the changes in cardiac activity induced by DNP: a) the enhanced repolarization (shortened APd) is attributed to an increase in membrane permeability to K+ associated with an enhanced K+ efflux; b) the decrease in the magnitude of the AP is ascribed either to an impaired active extrusion of Na+ or to a depression of the Na+-carrying system resulting in a decrease in Na+ influx; c) the depression in contractility is due to an interference with the transport, conversion, or utilization of ATP.