bluuebunny/crossref_metadata_2025_split huggingface dataset:
Extrinsic innervation of the canine abdominal vena cava and the origin of cholinergic vasoconstrictor nerves
Authors: Nakazato Y. , Ohga A. , Shigei T. , Uematsu T. 
Published: December 2014

1. The effects of electrical stimulation of the greater splanchnic nerve and the vagus nerve on the middle segment of the inferior vena cava (i.v.c.) were studied in anaesthetized and unilaterally or bilaterally adrenalectomized dogs. The vascular response of the segment was measured as the change in pressure of an intravascular cuff inserted into the lumen of the segment.2. Electrical stimulation of the greater splanchnic nerve of either side caused an increase in the tension of the vein with a delay of less than 3 sec. The tension increased with frequency of stimulation until it reached a maximum at the frequency of 32 Hz. The maximum tension development was consistently larger, by a factor of about two, when the right greater splanchnic nerve was stimulated than when the left was. It seems that the right greater splanchnic nerve supplies more sympathetic nerve fibres to the middle segment of the i.v.c. than does the left.3. The response to electrical stimulation of the right or left greater splanchnic nerve was markedly reduced by phentolamine or hexamethonium. The response remaining after treatment with phentolamine or hexamethonium was augmented by neostigmine and diminished by atropine.4. The electrical stimulation of the vagus nerve elicited no response of the vein before and after treatment with neostigmine.5. The effects of electrical stimulation of the right greater splanchnic nerve were further confirmed by a preparation in which the middle segment of the i.v.c. was perfused with Krebs solution in situ. The relation between the frequency of stimulation and the magnitude of the response was almost the same as in the in vivo experiments.6. It was also confirmed in the perfused preparation that the response to electrical stimulation of the right greater splanchnic nerve was reduced by phentolamine and the remaining response was augmented by neostigmine and abolished by atropine.7. Our data show that the middle segment of the canine i.v.c. receives both adrenergic and cholinergic excitatory innervation, preferentially via the right greater splanchnic nerve.8. The infrarenal segment of the i.v.c. was also examined in the in vivo experiment, in which it was shown that this segment received much clearer dominant innervation of the right greater splanchnic nerve.9. The infrarenal segment of the i.v.c. is also supplied with excitatory adrenergic fibres and, in some cases, with the cholinergic ones from the right greater splanchnic nerve.
Transport specificity for neutral and basic amino acids at maternal and fetal interfaces of the guinea‐pig placenta
Authors: Eaton B. M. , Mann G. E. , Yudilevich D. L. 
Published: December 2014

1. The unidirectional influx of amino acids into the guinea‐pig syncytiotrophoblast was measured using a single circulation paired‐tracer dilution technique which allows separate characterization of both fetal and maternal interfaces. An in situ preparation perfused through the fetal circulation was used to examine the fetal side, while an isolated preparation perfused through both the fetal and maternal circulations was used to study both interfaces simultaneously.2. On the fetal side the maximal uptake (Umax) determined at tracer concentrations was high for the short‐chain neutral amino acid alanine (76%) and the long‐chain neutrals, leucine (75%), phenylalanine (90%) and tyrosine (82%) and for the basic amino acid lysine (65%). In contrast, Umax was negligible for α‐methylaminoisobutyric acid and taurine, a β‐amino acid.3. The uptake of alanine and phenylalanine on the fetal side was inhibited by both short‐chain (alanine, serine, cysteine) and long‐chain (phenylalanine, methionine, leucine) neutral amino acids.
d‐alanine had no effect on
l‐alanine uptake whereas
d‐phenylalanine significantly inhibited that of
l‐phenylalanine. Diaminobutyric acid, lysine and arginine were effective inhibitors of alanine uptake but had no effect on phenylalanine uptake.4. On the maternal side uptake of alanine, phenylalanine and lysine was measured. Over a wide range of concentrations self‐inhibition of alanine influx was similar to the cross‐inhibition observed with phenylalanine. In contrast, the influx of phenylalanine, which was strongly self‐inhibited, was only partially cross‐inhibited by alanine.5. Influx of alanine and phenylalanine was measured at various perfusate concentrations and was found to be saturable on both maternal and fetal sides. The data were fitted to a single hyperbola and, on the maternal side, the Km for alanine (10.3±2.7 m
m, mean±
s.e., n = 3) was three‐fold higher than the value measured for phenylalanine (3·1±0·8 m
m). On the fetal side the Km values for alanine (8·4±1·4 m
m, n = 4) and phenylalanine (11·9±1·9 m
m, n = 3) were similar.6. The uptake of alanine, phenylalanine and lysine appeared to be highly sodium‐dependent accounting for 40‐70% of the total influx. However, the inhibited fractions were found to be different on the two sides of the placenta.7. The results of uptake, cross‐inhibition and Na+‐dependency experiments suggest the presence of an alanine‐serine‐cysteine (ASC) type system and a leucine (L) type system with markedly overlapping specificities at both the fetal and maternal interfaces. Separate kinetic characterization of a two carrier system was not possible under the conditions of these experiments. However, kinetic parameters for the over‐all transport of alanine and phenylalanine were measured.
Fusimotor reflexes in triceps surae elicited by natural stimulation of muscle afferents from the cat ipsilateral hind limb
Authors: Appelberg B. , Hulliger M. , Johansson H. , Sojka P. 
Published: December 2014

1. Experiments were performed in forty‐one cats anaesthetized with chloralose.2. The aim of the study was to investigate whether activity in stretch‐sensitive muscle receptors may cause reflex effects in fusimotor neurones.3. Activity in fusimotor neurones was studied indirectly by recording from primary and secondary muscle spindle afferents of the triceps surae muscle. The mean rate of firing of the afferents as well as either dynamic index (during ramp extension) or modulation (during sinusoidal extension) was determined. This was done under control conditions, with the posterior biceps—semitendinosus muscles relaxed, and under test conditions, with the same muscles extended.4. All together, seventy‐one primary afferents were studied quantitatively. Pure or predominantly dynamic effects were observed in twenty‐two, pure or predominantly static effects in nine and no statistically significant effects in forty of the units. Amongst seven secondary afferents studied, two showed weak fusimotor activation, the other five were not influenced.5. Electrical stimulation of the posterior biceps—semitendinosus or medial gastrocnemius nerves at group II strength was observed to cause dynamic fusimotor reflexes on a number of occasions.6. The reflex effects observed were, on many occasions, recorded in spinalized preparations.7. The reflex effects were not accompanied by any detectable e.m.g. activity in triceps, as judged from surface e.m.g. recordings. The reflex effects observed are therefore tentatively ascribed to activation of γ‐motoneurones, yet a contribution from β‐motoneurones cannot wholly be excluded.8. On the basis of available evidence concerning reflex connexions to γ‐motoneurones from various muscle afferents, it is suggested that the effects observed were caused by activation of muscle spindle secondary endings.
Further studies on the mechanism of phosphorylase activation in rabbit liver in response to splanchnic nerve stimulation
Authors: Shimazu Takashi , Usami Mihoko 
Published: December 2014

1. The mechanism of activation of liver phosphorylase after splanchnic nerve stimulation has been investigated in rabbits and compared with the effects of intraportal injections of noradrenaline.2. The increase in the activity of liver phosphorylase‐a, the active form of this key glycogenolytic enzyme, in response to injections of noradrenaline was blocked by β‐adrenergic antagonists, but not by α‐adrenergic antagonists, suggesting that the effect of noradrenaline is mediated mainly through β‐adrenoceptors in vivo. In contrast, the increase in phosphorylase activity in response to stimulation of the peripheral end of the splanchnic nerve was resistant to both α‐ and β‐adrenoceptor blockade.3. When diltiazem and verapamil, selective Ca2+ antagonists that restrict calcium influx across the cell membrane, were infused intraportally, the phosphorylase response to splanchnic nerve stimulation was virtually abolished, while the response to noradrenaline was unaltered.4. Infusion of the prostaglandin‐synthesis inhibitor indomethacin at a dose of 3·4 μg/min was found to block the activation of liver phosphorylase in response to stimulation of the splanchnic innervation.5. These results suggest that the mechanism whereby stimulation of the sympathetic innervation to the liver leads to activation of phosphorylase is not mediated by either α‐ or β‐adrenoceptors, but appears to depend upon prostaglandin formation and influx of Ca2+ ions into the hepatocytes.
Enhancement of ionic currents through voltage‐gated channels in the mouse oocyte after fertilization
Authors: Yamashita Naohide 
Published: December 2014

1. The changes of voltage‐gated ion channels in the mouse oocyte after fertilization were investigated under voltage clamp.2. About 60 min after introduction of sperm suspension into the fertilization medium, the amplitude of inward current through Ca2+‐channels increased, which occurred at anaphase during the second meiotic division. The peak amplitude of the maximum inward current per unit membrane capacity of the oocytes at metaphase was 20±3 μA/μF in 50 mM‐Sr medium. It was 28±8 μA/μF at anaphase, and 32±5 μA/μF at telophase. The kinetic properties as well as selectivity among Ca, Sr and Mn ions were not altered after fertilization.3. The outward surge current which was found at the higher membrane potential over +50 mV also increased in amplitude after fertilization, simultaneously with the increase in amplitude of inward current through Ca2+‐channels. The means and the standard deviations of the surge current per unit membrane capacity at 120 mV were 31±8 μA/μF at metaphase, and 48±7 μA/μF at telophase. The kinetic properties of the outward surge current were not altered after fertilization.4. Application of colcemid (10−7 mole/l.) or cytochalasin B (2 × 10−5 mole/l.) did not prevent the increase in amplitude of both inward current through Ca channels and the outward surge current.5. The membrane currents in N‐18 mouse neuroblastoma cells in logarithmic growth phase were examined under voltage clamp. The N‐18 neuroblastoma cells possessed the Ca inward current and the delayed outward current. The kinetic properties and the steady‐state inactivation of Ca2+‐channels in N‐18 neuroblastoma cells were compared with those in mouse oocytes. It was concluded that they could be regarded as identical between the mouse oocyte and the N‐18 neuroblastoma cell.
Osmotic water flow across the abdominal skin of the toad Bufo marinus: effect of vasopressin and isoprenaline
Authors: de Sousa R. C. , Grosso Alda 
Published: December 2014

1. Net water flow Jw, was measured across the abdominal skin of the toad Bufo marinus with a volumetric, automatic technique that allows for averaging Jw over time intervals as short as 1 sec.2. Basal Jw was very stable and corresponded to a coefficient of osmotic flow, LPD, of ca. 15 × 10−7 cm sec−1 atm−1 (or to an osmotic water permeability coefficient, Pf, of 20 μm sec−1).3. Both vasopressin and the β‐adrenergic agonist, isoprenaline, triggered high hydrosmotic responses that could lead to Pf values exceeding 250 μm sec−1. The effect of isoprenaline was very reproducible while that of vasopressin varied considerably.4. Methohexital and propranolol selectively inhibited the hydrosmotic effects of vasopressin and isoprenaline, respectively, whereas amiloride and ouabain had no effect.5. Mutual inhibition was found between vasopressin and isoprenaline in skins very sensitive to vasopressin. In less sensitive skins isoprenaline further increased Jw despite exposure of the epithelia to supramaximal concentrations of vasopressin.6. Differential reactivity to vasopressin was found between the skin and the bladder taken from the same toad. In some instances, the bladder responded normally to vasopressin while the skin was totally unresponsive, suggesting the presence of osmoregulatory mechanisms exerting a local modulation of the vasopressin action in different target epithelia of the same animal.
Adaptation of cardiac vagal responses to baroreceptor stimuli in the dog
Authors: Potter Erica K. 
Published: December 2014

1. There is adaptation of the cardiac vagal efferent responses to stimulation of the arterial baroreceptors by a series of brief intracarotid pressure pulses, by a sustained elevation of pulsatile systemic pressure, or by sustained steady increases in intracarotid pressure. This was demonstrated here in experiments on anaesthetized dogs.2. Trains of brief intracarotid pressure pulses were delivered to carotid baroreceptors at varying interstimulus intervals. Reflex bradycardia was evoked by the first stimulus of a train but as succeeding stimuli were placed closer to those preceding them they became less effective in evoking reflex bradycardia. This attenuation of the heart rate response was not due to attenuation of the responses of baroreceptor nerve endings to repeated brief stimuli, or to reflex changes in systemic blood pressure.3. Activity in single cardiac vagal efferent fibres was recorded in response to pairs of intracarotid pressure pulses, to step changes in non‐pulsatile carotid blood pressure, and to changes in pulsatile systemic blood pressure. Adaptation of cardiac vagal discharge over a period of 10 sec or more, to both pulsatile and non‐pulsatile increases in blood pressure, was shown.4. The slow time course of the adaptation of vagal discharge makes it most unlikely that it can be completely accounted for by adaptation of the baroreceptor nerve endings themselves. Therefore, the results obtained here are taken to indicate that adaptation occurs centrally, along the baroreceptor to vagal pathway.
Effects of nystatin‐mediated intracellular ion substitution on membrane currents in calf Purkinje fibres
Authors: Marban Eduardo , Tsien Richard W. 
Published: December 2014

1. Calf cardiac Purkinje fibres were exposed briefly to the ionophore nystatin to promote exchange of caesium for intracellular potassium. The effects of Cs loading were stable for at least 30 min, but they could be reversed by nystatin‐mediated K loading.2. After Cs loading, the resting potential shifted to about ‐20 mV and the current—voltage relationship showed a strong inhibition of inwardly rectifying K channels.3. Anodal break stimulation evoked normal action potential upstrokes and twitch contractions. The early repolarization (phase 1) was markedly slowed.4. Cs loading simplified the pattern of current changes evoked by step depolarizations over the plateau range. Membrane current reached an inward peak and then declined monotonically.5. The current signal showed no hint of the transient outward current found in untreated or K‐loaded preparations. Furthermore, Cs loading abolished the outward tails associated with deactivation of transient outward current, and occluded the blocking effect of the K‐channel inhibitor 4‐aminopyridine.6. Inhibition of transient outward current revealed a maximal inward current of about 5 μA/μF in 5·4 mM‐Cao, which is considerably larger than the net inward current without Cs loading.7. The inward current was attributed to Ca channels on the basis of its sensitivity to membrane potential, extracellular Ca, D600, Mn and Cd.8. Cs loading also reduced slow current changes associated with delayed rectification and pace‐maker depolarization.9. The results support the hypothesis that the transient outward current is carried by K+ ions, while providing a method for unmasking inward Ca current.
The development of the segmental pattern of skin sensory innervation in embryonic chick hind limb
Authors: Scott Sheryl A. 
Published: December 2014

1. The development of dermatomes in the chick hind limb was investigated with both electrophysiological recording from and horseradish peroxidase (HRP) labelling of neurones in lumbosacral dorsal root ganglia (d.r.g.s). The embryonic stages studied spanned the period before and after cell death.2. In mature embryos, after the bulk of cell death, physiological mapping showed that the location of the dermatome of each d.r.g. is consistent from embryo to embryo. HRP studies showed that axons from each d.r.g. project through the limb to the skin via a characteristic set of nerve trunks. Both the dermatomes and axonal projection pathways of adjacent d.r.g.s partially overlap one another, producing an orderly progression in the location of dermatomes and projection pathways along and within the limb, respectively.3. In younger embryos, before cell death, the location and amount of overlap of dermatomes, as well as the axonal projection pathways, are similar to the mature pattern. D.r.g.s that innervate distal skin on the shank and foot in mature embryos do not project out cutaneous nerve trunks in the thigh or contact nearby skin on the thigh at earlier stages.4. Axons from a single d.r.g. initially contact the skin at one or more characteristic spots; the dermatomes then enlarge, adding fine axonal branches.5. Carbon‐marking experiments showed that there are no large distal migrations of skin on the limb during the stages studied.6. Together these findings show that dermatomes on the chick hind limb do not develop by skin sensory axons simply growing to the nearest available skin, nor are axons towed to their final location by skin movements. Moreover, dermatomes are not shaped by cell death and the elimination of random or excessive axonal projections in the limb or the skin. It appears that skin sensory axons from each d.r.g. grow directly to their target skin along a defined set of pathways and establish their dermatome precisely at its characteristic location.
The electrogenic sodium pump in guinea‐pig ventricular muscle: inhibition of pump current by cardiac glycosides
Authors: Daut Jürgen , Rüdel Reinhardt 
Published: December 2014

1. The inhibition of the electrogenic sodium pump in guinea‐pig ventricular muscle by cardiac glycosides was studied with a voltage‐clamp technique.2. Superfusion of the preparation with dihydro‐ouabain (DHO) produced a reversible depolarization of up to 7 mV. When the membrane potential was clamped to a constant value near the resting potential application of DHO produced a corresponding current change in the inward direction which reached a steady state in less than 1 min.3. The drug‐induced current change (ID) was found to be the result of a parallel shift of the current—voltage relation. The contributions of a change in extracellular K or intracellular Na to the measured ID were shown to be very small. From these findings and the results summarized below it was concluded that ID represents the blockage of the electrogenic pump current by DHO and that it is proportional to the number of drug molecules bound to the Na—K‐ATPase in the intact cell.4. The dependence of ID on the concentration of DHO applied (5 × 10−6‐8 × 10−4 M) was found to be consistent with the predictions of the law of mass action for reversible one‐to‐one binding of the drug to the Na—K pump under equilibrium conditions. From a Scatchard‐type plot the equilibrium dissociation constant (KD) of DHO was determined to be 4·6 (±2·3) × 10−5 M.5. The steady‐state pump current in the resting preparation was calculated to be 0·81±0·26 μA/cm2. It contributed 6·4±0·9 mV to the resting potential in Tyrode solution containing 3 mM‐K.6. In the smallest preparations used the measured time course of the onset and decay of ID agreed with the chemical kinetics of binding and unbinding calculated for various DHO concentrations. The rate constant of unbinding (k2) was found to be 3·4 (±0·7) × 10−2 S−1 and the average rate constant of binding (k1) was 7·4 × 102 M−1 S−1.7. By comparing the effects of ouabain and DHO in the same preparation the following estimates of the chemical constants of ouabain binding to the Na—K pump were obtained: KD ≃ 1·5 × 10−6 M; k1 ≃ 4 × 103 M−1 S−1; k2 ≃ 6 × 10−3 S−1.8. An analysis of the transmembrane movements of Na and K in the steady state showed that the measured pump current density is consistent with a counter‐transport of 3 Na and 2 K ions.
Effects of a small serosal hydrostatic pressure on sodium and water transport and morphology in rabbit gall‐bladder
Authors: Eldrup E. , Frederiksen O. , Møllgård K. , Rostgaard J. 
Published: December 2014

1. In order to investigate the mechanism of serosal pressure‐induced inhibition of isosmotic fluid transport, the effect of 4·5 cm water serosal pressure on spontaneous water transfer (Jv) in rabbit gall‐bladders was measured (in the presence of a supporting soft nylon net on the mucosal side) in a modified Ussing chamber. This allowed unidirectional Na+ fluxes ([Formula: see text] and [Formula: see text]), transepithelial potential difference and resistance (Rt) to be measured simultaneously. The effects of the serosal pressure were also investigated by light and electron microscopy.2. During pressure application, Rt increased due to a covering effect of the mucosal support. The serosal pressure caused a parallel decrease in Jv and net Na+ transport ([Formula: see text]) across the free epithelial surface of 80‐85%. About 85% of the decrease in [Formula: see text] was due to a decrease in [Formula: see text].3. After inhibition of 93% of fluid absorption by serosal 10−3M‐ouabain, pressure‐induced change in Jv was only 8% of the spontaneous fluid transport rate.4. Control Na+ flux ratio ([Formula: see text]) was 3·5. The pressure‐induced increase in steady‐state [Formula: see text] of 30‐35% therefore contributed little to the decrease in [Formula: see text]. Further, this increase in [Formula: see text] was completely prevented by mucosal 10−3 M‐amiloride.5. All pressure‐induced effects on transport and electrical parameters were reversible.6. The light microscopical and scanning electron microscopical results showed that half of the epithelial surface was covered by the nylon net following serosal pressure application. Ruptures in the epithelium were not seen. Thin section and freeze fracture electron microscopy demonstrated continuous, well developed tight junctions both in control and experimental condition.7. It is concluded that a serosal pressure of only 4·5 cm water causes inhibition of a cellular active Na+ and water transport with only minimal, if any, contribution from paracellular filtration. This would seem incompatible with the concept that an active ion transport mechanism localized in the basolateral cell membrane is responsible for transepithelial fluid transport. The possibility of a mechanical fluid transport mechanism via elements of a tubulo‐cisternal endoplasmic reticulum is raised.