In frog atrial trabeculae low-Na contractures and caffeine contractures evoked in Na-poor solutions are increased by raising the external Ca concentration [( Ca]o), lowering the external Na concentration [( Na]o) or by tissue depolarization in K-rich fluids. The source of activator Ca for the low-Na and the caffeine contractures is probably different because Na-withdrawal contractures are inhibited by Mn2+ but unaffected by local anaesthetics, while the caffeine contractures are potentiated by Mn2+ and inhibited by local anaesthetics. The spontaneous relaxation of the low-Na contracture has a rate constant of 0.055 +/- 0.009 s-1, at room temperature for any [Na]o, [Ca]o or external K concentration [( K]o). The spontaneous relaxation of the caffeine contracture in Na-free fluid has a similar rate constant. However, the rate of spontaneous relaxation is increased if Na+ is present in the bathing medium and analysis of the results of experiments done in solutions with different [Na]o, [Ca]o or [K]o, suggests that two processes are involved in the reduction of the internal Ca concentration [( Ca]i) and the fall of tension. One, also responsible for the spontaneous relaxation of the low Na contracture, is dependent on metabolic energy and may be intracellular in origin. The other depends upon the activity of the sarcolemmal Na/Ca exchange, persists in the presence of metabolic inhibitors and is also activated during a low Na contracture when [Na]o is raised, or [Ca]o is lowered. The contractile response, of frog cardiac muscle to caffeine, would seem to be largely due to a release of Ca2+ from an intracellular store, but the strength of the resulting contracture depends upon a competition between the contractile proteins and the Na/Ca exchange for the released Ca2+.