Influence of the carotid sinus reflex on mean circulatory pressure was examined in anesthetized dogs with the vagus nerves intact. The carotid sinus reflex was elicited either by occlusion of the bilateral common carotid arteries (9 dogs) or by lowering intrasinus pressure of the isolated carotid sinuses (1 dog). When the reflex rise of arterial pressure was greater than 10mmHg, there also was an increase in mean circulatory pressure up to 2mmHg in 11 out of 20 instances. The increase in mean circulatory pressure tended to be greater as the reflex rise of mean arterial pressure was greater. Thus, when the pressor response was greater than 30mmHg, elevation of mean circulatory pressure was observed in 7 out of 8 cases. It is quite plausible that the control of cardiac output by the carotid sinus reflex is attributable, at least partly, to the Frank-Starling mechanism, since a reflex change in mean circulatory pressure will alter the venous return to the heart.

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Since HODGKIN et al.(1949) first recorded membrane ionic currents by the technique of voltage clamping the membrane of squid giant axons, it has been possible to predict precisely the ionic currents produced by an action potential. However, the ionic current produced during the propagating action potential can be obtained only after intricate experiments and laborious calculations. Employing the method used in the present report, the relationship between ionic currentand membrane potential of nerve and muscle fibers can easily be obtained. According to the cable equation, the ionic current is described as the difference between the first and second derivatives of the action potential. It is also calculated that the ionic current should be zero at the foot of the action potential. Applying this condition to the cable equation, the ionic current-membrane voltage relation can then be obtained from the electronically differentiated transmembrane action potential. The fact that this method can be applied to muscle fibers whose membrane structure is complicated due to the tubular system is also discussed.

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1. The effect on pregnant mouse of removing external Na was investigated by substituting sucrose, Tris, choline, and Li for Na. The membrane potential as well as the spike potential were not noticeably changed by a reduction of external Na to half (69mM Na) in Krebs solution. Although a reduction of Na to 15.5mM produced a slight depolarization, the amplitude of the action potentials was little affected. Reducing external Na to less than 5mM or to zero produced a prompt and sustained depolarization to-25mV, with cessation of spike activity and contracture. These observations are contrary to those expected from the Goldman equation.
2. Spike potentials were evoked by conditioning hyperpolarization for about 20 min in a Na-free solution. These then gradually diminished and eventually disappeared in 40min. Spontaneous spikes, which were abolished in Na- and Ca-free solution, reappeared upon subsequent addition of Ca (2.5mM).
3. The relationship between the amplitude of the action potential and the membrane potential, which was displaced by external current application, was investigated in normal and in low Na solutions. The relationship was S-shaped, with the amplitude of evoked action potentials decreasing at high membrane potentials. Its implication was discussed.
4. It was speculated that reduction of external Na inhibited the extrusion of Ca from the cell, hence producing a contracture in Na-free solution. Removal of external Na would therefore depolarize the membrane by changing the distribution of Ca across it. Alternatively, reduction of intracellular Na in Na-free solution may depress the electrogenic Na pump.

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1. The effect of catecholamines (adrenaline, noradrenaline, and isoprenaline) in combination with α- and β-blocking agents (phentolamine and propranolol) on pregnant mouse myometrium was investigated. The catecholamines had an inhibitory action in this tissue, the minimal dose required to produce inhibition being 3×10^-9 (g/ml) for isoprenaline, <10^-7 for adrenaline, and <10^-6 for noradrenaline. While β-adrenergic blocking agent antagonized the inhibitory action of the catecholamines, α-blocking agent did not.
2. Catecholamines produced a hyperpolarization of the membrane and hence spontaneous activity was inhibited. External current stimulation produced a spike potential with an amplitude comparable to that in Krebs solution. During hyperpolarization, there was no statistically significant change in membrane resistance, nor was there a difference between the effects of noradrenaline and isoprenaline.
3. When spontaneous activity was present in normal or low-Na (about 10mM) solution, isoprenaline (10^-8g/ml) abolished it. Depolarization and contracture evoked in zero Na (replacement with Tris or sucrose) were restored to normal by isoprenaline, and a spike potential was evoked which was bigger than that in Krebs solution. The existence of external Ca was essential to production of the repolarization.
4. From the above results, a tentative hypothesis on the mechanism of action of catecholamines on pregnant mouse uterus was made as follows:(i) Hyperpolarization, which is responsible for the inhibitory action, is due either to an acceleration of electrogenic Na pumping or to a change in the interaction between the membrane and extracellular, as well as intracellular, Ca.(ii) Isoprenaline reduces [Ca] _i, hence abolishing the contracture in zero Na. This may also lead to the production of an action potential in Na-free solution.

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Some characteristics of synaptic potentials arising in the large cells of the lobster cardiac ganglion were investigated by means of intracellular recording and current injection.
1. The spontaneous burst was mainly composed of two kinds of synaptic potentials differing in various features, indicating that the large cells were innervated by two common presynaptic nerve fibers from pacemakers.
2. Antifacilitation was observed in large synaptic potentials, while it was not observed in small synaptic potentials.
3. Depolarization of the large cell accelerated the initiation of large synaptic potentials, andhyperpolarization impeded it. The electrotonic interaction between large cells and the presynaptic nerve cells, which produce large synaptic potentials, was rather strong.
4. Polarization of the large cell had less effect on the initiation of small synaptic potentials than on that of large synapticpotentials; the electrotonic interaction between large cells and the presynaptic nerve cells, which produce small synaptic potentials, was exceedingly weak.
5. A brief current pulse applied to the large cell evoked the slow potential, which was separated from a train of small synaptic potentials. The positive feedback of the slow potential was demonstrated well.
6. Repetitive small synaptic potentials had an acceleratory effect on the burst initiation. The rate of slow depolarization increased with development of small synaptic potentials.
7. Two types of presynaptic nerve cells exhibited differences in time courses of repetitive discharges; one produced a brief train of discharges, and the other an extensive train.
8. It was concluded that the large cells are controlled by two types of presynaptic nervecells; one evokes large synaptic potentials, initiating impulses, and the other induces small synaptic potentials, increasing excitability of the postsynaptic membrane. The latter controls the former. The large cell behaves as a pacemaker when presynaptic nerve cells become inactive or when their activities are delayed.

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When palmar skin potential level (SPL) is recorded during periods of minimal arousal sweating, and a concentration of potassium chloride within physiological limits is used for the external electrolyte, the value of the “basal” SPL (BSPL) recorded can be expressed as a function of the external/epidermal potassium concentration gradient.
The present study reports comparison of BSPL values obtained with the use of physiologically comparable concentrations of sodium and potassium chlorides. The results suggest the possibility that the BSPL methodology may provide a means of monitoring electrolyte shifts in the human subject.
In addition, sex differences in BSPL values were demonstrated.

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The potentiating effect of disodium 2-methyl mercapto-5'-inosinate (Mes-IMP) on gustatory responses to monosodium glutamate (MSG) was examined and compared with those of sodium 5'-inosinate (5'-IMP) and sodium 5'-guanylate (5'-GMP) by recording responses in the whole chorda tympani nerve and in single gustatory fibers in rats. Mes-IMP had a lower threshold for response than 5'-IMP. Addition of 0.0001% Mes-IMP to 0.3% MSG yielded significant enhancement in the response. The enhancement produced by Mes-IMP was nearly equal to that shown by 5'-IMP of an amount ten times greater. The enhancement was predominantly observed in fibers responsive to sucrose. The magnitude of the enhancement, produced by the addition of a fixed amount of Mes-IMP to MSG of varying concentrations, was greater at MSG concentrations below 0.03 M than at higher concentrations.

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Measurements of aerobic capacity by three different work tests, namely two cycling tests with pedal frequencies of 60 and 50 rpm respectively and a treadmill walk test, were carried out on 8 male Japanese students studying at the University of California at Santa Barbara. The maximal oxygen uptake (max V_o2) for all three tests was not significantly different (P>0.05). However, ventilatory parameters reflected differing patterns by which the max V_o2 was obtained. The study data indicated that cycling exercises at a pedaling frequency of 60 rpm produced excessive hyperventilation leading to syncope during recovery from exercise.

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Effects of externally applied noradrenaline and isoprenaline on the electrical and mechanical activities of the guinea-pig was deferens were observed using the double sucrose gap method.
1. Noradrenaline (10^-8-10^-5g/ml) depolarized the membrane, reduced the membrane resistance, produced spike generation and brought about contraction (α-response). These effects were suppressed by treatment with phentolamine (10^-6-10^-5g/ml).
2. The α-response is caused by increased Na and K conductances, and probably by increased Ca conductance also. The Cl ion reduced the α-response due to high conductance of the membrane.
3. Isoprenaline (10^-7-10^-8g/ml) neither depolarized the membrane nor changed the membrane resistance but reduced the amplitude of the phasic contraction (β-response) evoked by an outward current pulse. The suppression of the contraction was blocked by treatment with propranolol (10^-6g/ml).
4. Ouabain (10^-6g/ml) depolarized the membrane, reduced the membrane resistance and increased the spike frequency. Under the above conditions, effects of catecholamines were not suppressed.
5. The relationships between the membrane potential and tension development were observed using the microelectrode and double sucrose gap methods. The amplitudes of the phasic response of the contracture were closely related to membrane potential levels displaced by excess K ion, but the amplitudes of the tonic response were not related.
6. In excess K-Krebs solution (below 59mM), noradrenaline (10^-7-10^-6g/ml) and isoprenaline (10^-7-10^-6g/ml) were similar to those observed in 5.9mM K-Krebs. When external Na ion was removed, however, the effects of noradrenaline and isoprenaline were absent.
7. If K-Krebs solution was in excess (above 59mM), the amplitude of the tonic response of the contracture was less than 20% of the amplitude of the phasic response. Noradrenaline (10^-8-10^-9g/ml) and isoprenaline (10^-6-10^-5g/ml) did not have any marked effect on electrical and mechanical properties of the muscle.
8. Acetylcholine (10^-7-10^-6g/ml) had effects similar to those of noradrenaline on the normal and depolarized muscle.
9. Possible actions of noradrenaline and isoprenaline in the normal and depolarized muscles were discussed in relation to the electrical and mechanical properties of the guinea-pig taenia coli.

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