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1. The tension generated by isolated frog atrial trabecules, during exposure to solutions containing a high potassium concentration, is not maintained but spontaneously relaxes. The final part of this relaxation can be fitted by a single exponential function.

2. The recovery of the tension generating mechanisms following the spontaneous relaxation of a potassium contracture depends on the preceding membrane potential and the time since the last contracture.

3. The rate of the exponential phase of the spontaneous relaxation is independent of the [K]_o and hence the membrane potential, the [Ca]_o; and when the [Ca]_o/[Na]_o² ratio is maintained it is also independent of the [Na]_o. This relaxation is not influenced by atropine or pronethalol.

4. When sodium is totally excluded from the bathing medium the rate of relaxation of a later potassium contracture is much increased. It is argued that this change is due to a fall in the intracellular sodium concentration.

5. The consequences of these results are discussed, and the hypothesis that is favoured would require that contraction is induced by a transient release of calcium into the sarcoplasm, probably triggered by a potential dependent, and probably also transient, influx of calcium through the cell membrane. Relaxation is supposed to occur when this activator-calcium is then removed by an intracellular relaxing system that resembles the sarcoplasmic reticulum of other muscles. What this intracellular structure might be, is also discussed.