1. The effects of concentration of constituent ions of Tyrode solution on the membrane potentials and mechanical events were studied on the ventricular muscle of rabbits.
2. When NaCl was less or KCl was more than normal, the plateau level lowered and the duration became shorter as expected. Vice versa, when NaCl was more or KCl was less than normal, the reverse effects were observed. These changes appeared more rapidly and conspicuously in Ca-deficient condition.
3. Substitution of I^-, NO₃^- or Br^- for Cl^- had little effects both on the membrane potentials and tensions. Accordingly, most of the effects of NaCl or KCl concentration were considered attributable to each cations.
4. Even in K⁺ deficient condition and in all other cases examined, the plateau could not appear without Nat. Therefore, Na⁺ is indispensable for producing the plateau.
5. Na⁺ or K⁺ removal within the limit of 3/4 of normal improved the twitch tension conspicuously.
6. Depletion of Cl^- did not produce any appreciable potentiation of contraction as observed in skeletal muscle.
7. Ca⁺⁺ was only cation in Tyrode solution, the removal of which caused a straight and complete disappearance of the contraction.
8. Mg⁺⁺ did not produce any eminent effects on the membrane potentials except the shortening of action potential, but caused an increase of resting tension and a decrease of contraction in both cases of excess and lack of the ions.
9. Differences between the effects of various ions on the cardiac and skeletal muscles were discussed, and difficulties to relate the potentials to the mechanical events were pointed out.

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1. The effects of EDTA on the transmembrane potentials and mechanical events of the ventricular muscle of rabbits were studied under different ionic conditions.
2. EDTA (5×10^-3M) caused a relaxation and complete disappearance of the contraction in spite of the appearance of slight depolarization of the membrane, and marked prolongation in duration of the action potential. An increase of the latent period and a rise in threshold were also noticed before automaticity of the muscle occurred.
3. After reintroducing of normal Tyrode solution, small oscillation appeared on the plateau and developed to a full repolarization of the membrane, when exceeded a critical value. The potential, soon returning up to the plateau from the resting potential level, shifted between these two stable states spontaneously and repeatedly.
4. When EDTA was added to and NaCl was depleted from the solution, the level of plateau lowered and the duration rather shortened despite the action of EDTA. The lowering of spike height was continuous but the plateau potential stayed for a while at a level about-17mV and later diminished. Under these conditions the action potential appeared often divided into two components, spike and plateau.
5. When EDTA was added and KCl was depleted from the solution, the prolongation of plateau was more remarkable than when EDTA alone applied. But the prolongation was canceled and rather a shortening of the plateau appeared when Na⁺ was lack in the solution. Oscillation of increasing amplitude was also observed toward the end of plateau when the KCl-lack EDTA solution was replaced by normal one.
6. EDTA-added NaCl-excess Tyrode caused first an increase in height of both the spike and plateau and then a decrease probably due to the hypertonicity of solution. EDTA-added KCl-excess Tyrode, on the other hand, produced a decrease of the spike and later the plateau.
7. From these results it is assumed that the transmembrane action potential of the cardiac muscle has at least two components, spike and plateau, each of which relates principally but differently to Na⁺ ions. The plateau potential was further estimated to have some relation with Ca⁺⁺-chelating action on the membrane of the contractile elements of the muscle during the tension development.

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1. Effects of afferent vagal stimulation were observed on medullary respiratory discharges of urethanized rabbits.
2. In a weak inspiratory response caused by low-frequency stimulation, inspiratory bursts gave way to a continuous firing, the frequency of which, however, remained unchanged compared with that of control inspiratory discharges. The discharge intervals of expiratory neurones were prolonged.
3. In a strong expiratory response caused by high-frequency stimulation, inspiratory discharges were abolished completely. Changes of expiratory discharges were identical with those of inspiratory discharge in inspiratory response mentioned above.
4. In a respiratory acceleration, both inspiratory and expiratory discharges were inhibited numbers of firing per bursts were decreased remarkably and their discharge intervals were prolonged.
5. Based on these results, the conclusion was drawn that the inspiratory and expiratory responses to low- and high-frequency vagal stimulation were brought about by inhibition of expiratory and inspiratory neurones respectively.

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1. A sudden increase of the external potassium concentration, [K] ₀, from 5 to 80.7 mM-K caused a retractor pharynx muscle (RPM) of the snail to develop a tension of about 2.5 kg/cm² related to log [K] ₀ by a steep S-shape curve.
2. The potassium contracture tension of the muscle was reduced and eventually eliminated when the muscle was kept in calcium-free solution. The time course for this inhibition was determined by the rate that calcium ions diffuse out from the extracellular space of the muscle to bathing fluid.
3. Calcium concentration in Ringer's solution affected the magnitude of contractile response, not only contracture tension produced by potassium but also twitch tension elicited directly or indirectly; the response increased up to about 13.1 mM-Ca and decreased with a further increase in concentration.
4. Calcium and sodium affected the twitch tension of the muscle produced by direct and indirect stimulations in an antagonistic way and the tension was related to the ratio [Ca²⁺]:[Na+] 2 in the range of 3-20×10^-4 mM^-1, but the relation could not be observed on the contracture tension produced by potassium.

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Action potentials of oyster myocardium recorded with suction electrodes showed a similar pattern to that obtained by the intracellular microelectrodes and their patterns were comparable to the action potentials of the vertebrate smooth muscles. When sea water was replaced by the isotonic sucrose solution the spontaneous activities eventually ceased, but were restored when the heart was returned to sea water. The activities were also restored when the sucrose solution contained either Na⁺, K⁺, Sr⁺⁺ or Ba⁺⁺. It was suggested that the ionic mechanisms responsible for the initiation of action potential may not be very specific in oyster myocardium, although Na⁺ may play a major role in the normal condition. Contrary to the vertebrate smooth muscles, Ca⁺⁺ inhibited a pacemaker activity of the oyster myocardium, therefore, no spontaneous contractions could be observed in CaCl₂-sucrose solution.

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1. In neurohypophysectomized rats 7 days postoperative, adrenal ascorbic acid depletion following epinephrine was almost entirely abolished and the increase in adrenal and plasma corticosterone was not statistically significant as compared with the resting levels of this group.
2. Neurohypophysectomized rats 14 days postoperative responded to epinephrine as normal rats in corticosterone release, but adrenal ascorbic acid response was slightly reduced.
3. Administration of epinephrine into normal rats caused a marked decrease in the anterior lobe ACTH content, but a slight decrease in the posterior lobe ACTH.
4. Adrenocortical response to exogenous ACTH was of the same extent in both neurohypophysectomized and control rats.

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In order to elucidate the relation of the ureteral motility to ureteral ganglion cells, the ureteral lumen of dogs anesthetized with pentobarbital sodium is perfused with saline solution, or with the saline solution to which acid or alkali is added in various concentrations.
1. In the orthodromic perfusion the following facts are noted:
a) When the counter pressure is kept constant, the outflow volume per unit time interval increases with increase in the pressure gradient.
b) When the counter pressure is lower than a certain critical point, the pressure gradient just necessary enough to produce the outflow, i. e. the threshold pressure gradient, is lowered with increase in the counter pressure. Besides, at the same pressure gradient, the higher the counter pressure is, the greater the amount of the outflow volume.
c) When the counter pressure rises beyond a critical pressure, there occurs a retardation of the flow, which then becomes more and more distinct with further increase in the counter pressure, threshold pressure gradient tending to become higher again. After all it may be concluded that with increase in the counter pressure the caliber of the ureter is widened gradually until a certain critical pressure is reached, and then narrowed again when the pressure is further increased beyond the critical point.
2. In the condition where both the counter pressure and the pressure gradient are within the moderate range, the flow instantaneously stops when the direction of the perfusion is reversed. It is observed that, while the flow stops, the lower part of the ureter falls into a persistent contraction superimposed with pulsations that propagate as waves both up- and downwards.
3. Comparing the results described above with those obtained in the perfusion experiment of the small intestine, it can be concluded that the ureteral ganglion cells have no particular function in the ureteral motility, and that the change of the ureteral motility observed in the ortho- and antidromic perfusion of the ureteral lumen is entirely of myogenic origin.

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1. In the dog anesthetized with pentobarbital sodium the unilateral ureter was extraperitoneally exposed and to three localized regions in the upper, middle and lower parts were applied the plethysmographic tambours which enabled to record the ureteral motility without disturbing the flow of urine.
2. It is often noted that the peristalses recur at a fairly rapid succession (period: 3.4±0.9 sec.) and in uniform amplitude.
3. When the peristalses are produced at an exceedingly rapid succession (period: 2.4±0.3 sec.) in the pace maker region, every other peristalsis is reduced in strength or abolished in the lower part.
4. The electric stimulation of the extraureteral sympathetic as well as parasympathetic nerves always produces on the ureter the increase of tone accompanied with the acceleration of the rate of peristalses. However, the regional difference is noted as to the degree of excitation. a) As to the rate of the peristalses the pronounced accelerating effect is produced by stimulating the splanchnic nerve, and the vagal, hypogastric and pelvic nerve show the effect much less than that obtained by splanchnic stimulation. b) As to the muscle tone the splanchnic nerve exerts in particular the remarkable influence on the upper part of the ureter, while the hypogastric as well as the pelvic nerve has the influence especially on the lower part, and the effect of the vagus nerve is of only a slight degree through the whole length of the ureter.
5. Both adrenaline and acetylcholine exert on the ureteral motility the excitatory actions essentially similar to those obtained by stimulating the extraureteral sympathetic as well as parasympathetic nerves.
6. Both atropine and hexamethonium depress the ureteral motility. Morphine exerts the excitatory action on the ureteral motility.
7. From the results described in 4 and 5 it may be concluded that both sympathetic and parasympathetic nerves lack opposing action on the ureteral motility.

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1. Characteristics of structure in the sympathetic neuron of amphibia were reported. A neuron and its satellite cell in the sympathetic ganglion of frog and toad form a peculiar shape which resembles to the octopus.
2. Two types of synaptic vesicles were differentiated. One has a peak at 500Å in size distribution curve, and the other at 1, 000Å. The vesicles of the latter have dense cores.
3. Adrenergic transmission mechanism in the sympathetic ganglion was suggested, at least in some of the neurons in it.

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