Contraction in frog atrial trabecules is likely induced by a transient release of calcium into the sarcoplasm, with relaxation occurring via an intracellular relaxing system.
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No immediate clinical implications; supports intracellular relaxation mechanisms but leaves open mammalian translation.
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](o) (2) 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.
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Reg Chapman (1973) studied this question.
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