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The effects of hypotonic solution on the mechanical activities and action potential of the bullfrog atrium were investigated. Exposure of muscle to hypotonic solutions (70 % of normal solution) produced initially a transient increase in twitch after which twitch declined below the control level. The response is independent of the kinds of salts withdrawn to make the medium hypotonic and of the presence of betablocker (S x 10-7 M propranolol). The resting potential and the plateau level of action potential were little changed initially. When the twitch declined, a small amount of depolarization and a shortening of action potential duration were observed; however, the plateau level of action potential was not reduced. The initial increase in twitch was not observed, and only the gradual decline of twitch remained in the caffeine containing hypotonic solution. The weight of muscle increased 10% in the hypotonic solution. The resting tension was also increased trasiently and then declined to reach a maintained plateau with exposure to hypotonic solution. In the 0-Ca2+ or caffeine containing medium, the transient component of contracture was suppressed but the plateau tension remained. It is suggested that the initial transient increase of twitch by the perfusion of the hypotonic solution was induced by the Ca2+ released from the sarcoplasmic reticulum (SR), and the resultant decline of twitch resulted from the depletion of Ca2+ from the SR and/or from the shortening of action potential duration.

Lanthanum of 0.1 to 0.2 mM caused a twitch inhibition and further showed a marked, long-lasting twitch potentiation during washout in both ventricular strips of bullfrog and atrial or papillary muscles of guinea-pig. It was found that the effect was more conspicuous in the frog heart. A similar potentiation was observed by applying gadolinium instead of lanthanum. The participation of endogeneous catecholamine release is unlikely since the positive inotropic effect was never affected by the presence of Q-adrenergic blocker. The potentiation was not accompanied by any increase in the action potential plateau, suggesting independence of the phenomenonr on the calcium current. A marked elevation of the resting tension was produced during a long-term lanthanum perfusion, reflecting the increase in the intracellular calcium level. On the other hand, transient increase in the resting tension was frequently observed on returning to normal Ringer solution. The latter change seemed to result from a transient increase in the resting permeability to calcium ions. The negative or positive inotropic effect by increasing or lowering the external sodium concentration observed under the control condition was strongly depressed during the twitch potentiation. In addition, sodium-free contracture induced by solutions isotonically replaced with sucrose or potassium chloride was augmented both during lanthanum perfusion and during its washout. These results suggest the possibility that the elevation of the intracellular calcium level due to inhibition of Na-Ca exchange mechanism and/or increase in the calcium permeability is the principal cause for the twitch potentiation caused by lanthanum washout.

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