Some factors which may influence the high-K-induced contracture of guinea-pig vas deferens were studied.Portional variations were observed in the height of tonic contraction but not in phasic contraction; tonic contraction was higher on the epididymal side and lower on the prostatic side.Circular muscle showed contracture similar to that of longitudinal muscle in the shapes of the contrature and the tendency to portional variations.Histological variations of muscle structure could not explain these variations.
Electrical stimulation of the preparation by continuous weak AC current induced contracture similar to the high-K-induced contracture.The contracture evoked by AC stimulation was blocked by TTX and phentolamine.
Blocking agents of possible transmission involved in high-K depolarization did not alter the relation of phasic and tonic contractions, although some of the drugs showed an inhibiting and some an enhancing effect. In isotonic observations, tonic contraction was highly sensitive to load and was elevated with a low load and depressed with a high load.
It was revealed that the phasic and tonic contraction of high-K-induced contracture was a direct reaction of longitudinal muscle, although various factors could have had some influence on the contracture.

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The role of Ca in phasic and tonic contractions of high-Kinduced contractures of guinea-pig vas deferens was studied.It was shown that phasic contraction was initiated by a burst of action potentials, and tonic contraction by sustained depolarization.Phasic contraction seemed to be related to the rate and degree of depolarization, whereas tonic contraction seemed to be related only to the degree of depolarization.
Tonic contraction was more sensitive to a reduction of extracellular Ca, though both types of contraction were abolished by Ca removal.The. tonic contraction observed with isotonic recording was more sensitive to extracellular Ca than that observed with isometric recording.Maximum contractions were achieved with lower Ca than that in isometric measurement.Verapamil blocked tonic contraction at a low concentration, and both contractions at a high concentration.Mn or La blocked the phasic and tonic contractions first.After prolonged exposure to either ion, however, tonic contraction could be induced.The results suggest that both phasic and tonic contractions were induced by Ca-influx through the cell membrane, and that tonic contraction was maintained by a constantly elevated intracellular Ca concentration which is the consequence of an altered equilibration of Ca influx and Ca extrusion through the cell membrane.

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Electron microscopic studies on the ultrastructural changes of the sarcoplasmic reticulum (SR) of the skeletal muscle were performed during caffeine rapid cooling contracture (RCC).The swelling of the SR was clearly induced by RCC.The diameter of the SR fixed for the electron microscopic study at the peak tension of RCC increased with graded caffeine concentration.Mean diameters of the SR (terminal cisternae) were (29.42±9.27)×10_-2μm at 1mM, (31.37±10.68)×10_-2 μm at 2mM, (35.33±8.60)×10_-2μm at 4mM caffbine, respectively, and (20.71±6.94)×10_-2μm at peak tetanus.On returning to room temperature (after RCC), the enlarged SR by RCC returned to its initial state (ca.19×10_-2μm) except in the case of RCC at 4mM caffeine concentration level.Rupture of the SR and other irreversible changes during RCC occurred at 4mM caffeine concentration level.On the other hand, there were no remarkable alterations in ultrastructure of the SR in tetanus.No morphological changes were observed at the SR-T tubule junction (junctional gap) or in the intra-SR granules (globular particles) during RCC and tetanus.It might be suggested that the morphological changes of the SR on caffeine rapid cooling associated with Ca released from the SR.

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Effects of temperature stimuli on plasma glucagon levels were studied in fasted (18hr) and shorn rats.Plasma glucagon levels rose significantly on exposures to both cold (-5°C, 60min)(p<0.001) and heat (36°C, 60min)(p<0.001) from that in control rats at 25°C.Cold stimulus increased blood FFA level (p<0.001) and both cold and heat stimuli increased blood glycerol levels (p<0.05-0.001).FFA/glycerol molar ratio decreased to a similar extent on both cold and heat exposures (p<0.02-0.01).It was noted that plasma glucagon, blood FFA and glycerol levels increased significantly more in cold-exposed rats (p<0.001) than in heat-exposed ones.There were positive relations of plasma glucagon levels to blood FFA and glycerol levels (p<0.001), while an inverse relation of plasma glucagon level to FFA/glycerol molar ratio was observed in all experimental rats (p<0.05).Cold exposure reduced blood glucose level (p<0.001), while heat exposure did not affect it.Cold-induced increases of plasma glucagon and blood FFA levels were diminished significantly in cold-acclimated rats as compared with those in controls (p<0.05-0.001).Blood glycerol increased and FFA/glycerol molar ratio decreased to a similar extent on cold exposure in both control and cold-acclimated rats.Correlation between plasma glucagon and FFA/glvcerol molar ratio was inversely significant in controls, but not significant in cold-acclimated rats.Blood glucose level was not altered on cold exposure in cold-acclimated rats.It was concluded that acute exposures to temperature stimuli, especially to cold, stimulate glucagon release, accompanied by increased utilization and mobilization of FFA and glucose, and plasma glucagon response to cold is diminished due to cold acclimation.

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Using the HRP method, we studied cardiac and non-cardiac preganglionic neurones of the thoracic vagus nerve in the cat.The inferior cardiac branches of the right thoracic vagus nerve were differentiated from the neighboring non-cardiac branches by positive cardiac slowing following electrical stimulation.A small amount of crystalline HRP was placed at the central cut end of the cardiac or non-cardiac branches.After a survival period of 2 days, the medulla oblongata, the stellate ganglion (SG), the superior cervical (SCG) and the nodose ganglion (NG) were serially sectioned and processed for histochemical demonstration of HRP.
In the medulla oblongata, HRP-labeled cells were mainly located in 2 regions:(1) within and around the ambiguus complex (site A);(2) within the dorsal vagus nucleus (site X).After applying HRP to the cardiac branches, 968 HRP-labeled cells were observed in 7 animals bilaterally with the ipsilateral dominance (94%);81% of them were found in site A. After applying HRP to the non-cardiac branches, 447 HRP-labeled cells were seen in 2 animals bilaterally with the ipsilateral dominance (92%); 79% of them were found in site X.
Many HRP-labeled cells were found in the SG and NG, indicating that the cardiac branches are composed of sensory afferent and sympathetic efferent fibres as well as cardiac vagus efferent fibres.

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To assess overall bodily transvascular fluid flow due to osmotic imbalance between blood and interstitial fluid during or after addition of hypertonic saline, sugar-, albumin-and dextran solutions or CO₂ mixture to blood, arterial blood colloid osmotic pressure (COP) of anesthetized dogs was continuously measured with a needle-type colloid osmometer.Plasma volume change (ΔV_p) was estimated from the changes in either the equivalent albumin concentration (C) or the albumin concentration equivalent to plasma COP, which was well confirmed in inanimate model experiments.Carbon dioxide inhalation caused RBC swelling (1.5% volume increase/10mmHg of P_CO2).Intravenous injection of hypertonic solutions resulted in transient osmotic flow (8.5±2.2ml/g of solute per kg of animal weight by NaCl, and 1.7±0.4 by glucose), and albumin and dextran also induced fluid flow (1.3±0.4 by albumin and 2.2±0.7 by dextran), which depended on van't Hoff's law and reflection coefficient of solutes.

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The membrane of bullfrog atrial muscle is hyperpolarized by an increase of K⁺ conductance in carbachol-containing Ringer solution. The present experiment demonstrated that both the membrane hyperpolarization and K⁺ conductance increase showed a decay during prolonged application of carbachol, suggesting desensitization of the muscarinic receptor.Such a decay of the membrane conductance increase was also observed when the membrane potential was clamped at the level of the K⁺ equilibrium potential;no net flow of K⁺ across the membrane was expected under such a condition.When carbachol was withdrawn from the external solution after its application for 5-10min, both the membrane potential and conductance quickly returned to normal control values within 3-4min, suggesting that the ionic distribution across the membrane also returned to normal.Under such a condition, however, the response to a second application of carbachol was depressed for an extended period.Similarly, decay of the response was observed when carbachol was applied repeatedly for a short period with a short time interval.These results suggested that the muscarinic receptor of the present preparation shows desensitization to carbachol. Similar results were obtained with acetylcholine.The rate of onset of desensitization to carbachol was very slow compared with that of the end-plate;the half-time was 6.62±2.24min (mean±SD, n=13).This rate, however, was dependent on the membrane potential level and the Ca²⁺concentration in the external solution, as in the case of the endplate, suggesting that the molecular mechanism of desensitization occurring at the receptor-ionic channel complex of the muscarinic receptor of the atrial muscle was comparable with that of the nicotinic receptor of the end-plate.

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In previous studies, when rabbit cortical collecting ducts were studied under standard conditions in vitro, bicarbonate transport was conditioned by the acid-base status in vivo of the animals from which the tubules were obtained.The collecting ducts absorbed bicarbonate if the animals were acidotic (from ammonium chloride administration), but they secreted bicarbonate if the animals were alkalotic (from sodium bicarbonate administration).The purpose of the present studies was to test whether similar conditioning occurs in other nephron segments.In proximal straight tubules neither the sodium-dependent nor the sodium-independent component of bicarbonate absorption was significantly affected by the acid-base status of the animals from which the tubules were obtained.In cortical thick ascending limbs, chloride was absorbed, but there was no net transport of bicarbonate by tubules whether they came from acidotic or alkalotic animals.
Since cortical thick ascending limbs were not found to transport bicarbonate, they cannot be implicated in the control of bicarbonate excretion. We conclude that the previously observed conditioning of bicarbonate transport occurs in collecting ducts but not in proximal straight tubules or in cortical thick ascending limbs in the same experimental situation.

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The relation between membrane potential and Ca²⁺fluxes in the skeletal fragmented sarcoplasmic reticulum (FSR) was investigated using cyanine dye (diS-C₃-(5)) as a potential probe.Change of membrane potential and Ca²⁺release from FSR were induced by changing the ionic composition of the medium.
When the medium was changed from K-gluconate to Tris-gluconate, a large fluorescence intensity change was observed, while no Ca²⁺release occurred.On the other hand, when the medium was changed from K-gluconate to KCl, Ca²⁺release occurred notwithstanding a relatively small fluorescence intensity change.This KCl-induced Ca²⁺release from FSR was inhibited by the addition of sucrose.Also, the presence of both permeable anion and cation was required for induction of Ca²⁺ release. These results suggest that there is no correlation between “depolarization” and Ca²⁺release.
Ca²⁺uptake by FSR created the positive-inside potential which was reversed by the application of Cat+ionophore A23187.The addition of valinomycin or nigericin, and the replacement of Cl^-with gluconate^-affected potential formation.These facts suggest that Cat+uptake is accompanied by K⁺efflux and/or Cl^-influx for partial compensation of the change.

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The hyperbolic force-velocity relation was obtained by afterload method for the tetanic contraction of frog atrial muscle.The dynamic constants (a/F_m and b), the maximum velocity and especially the maximum tension were considerably smaller than those of ventricular muscle.

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Dermally applied ouabain decreased the short circuit current (SCC) in frog skin, whereas epidermal cadmium increased it.The percent increase in SCC induced by Cd²⁺was never modified by the presence of ouabain.This suggests that Cd²⁺and ouabain may exert their effects on Na transport independently.

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