bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of vasopressin in blood pressure regulation immediately following acute haemorrhage in the rat
Authors: Laycock J. F. , Penn W. , Shirley D. G. , Walter S. J. 
Published: December 2014

1. The possible pressor effect of vasopressin immediately after acute haemorrhage has been studied using anaesthetized Brattleboro rats with diabetes insipidus and rats of the Long Evans parent strain.2. A blood loss of 0·5% of the body weight caused a significant decrease in mean arterial blood pressure, measured 10 min later, in Brattleboro rats, whereas this degree of haemorrhage was non‐hypotensive in the control Long Evans rats. Following subsequent blood losses (each of 0·5% of the body weight), mean arterial blood pressure in Brattleboro rats was always significantly lower than in Long Evans rats.3. While no antidiuretic activity was at any time found in the plasma of Brattleboro rats, haemorrhages greater than 1% of the body weight were associated with marked increases in plasma arginine vasopressin (AVP) of Long Evans rats.4. When Brattleboro and Long Evans rats were subjected to a single haemorrhage of 2% of the body weight, the immediate decrease in arterial blood pressure was similar in the two groups. However, 5 and 10 min after the haemorrhage the arterial blood pressure was significantly higher in the Long Evans rats. When vasopressin was infused into Brattleboro rats so that plasma levels of the hormone approached those found in Long Evans rats, the mean arterial blood pressure 0, 5 and 10 min after haemorrhage was similar to that in the Long Evans animals.5. It is concluded that in the anaesthetized rat, vasopressin plays an important role in the regulation of arterial blood pressure during the period immediately following acute haemorrhage.
The effects of renal denervation and meclofenamate on renal blood flow regulation in conscious rabbits
Authors: Beilin L. J. , Bhattacharya J. 
Published: December 2014

1. The effect on renal blood flow regulation of unilateral renal denervation followed by administration of a prostaglandin synthesis inhibitor has been studied in nine conscious rabbits.2. Renal blood flow distribution was estimated using radioactive microspheres injected via a pre‐implanted left ventricular cannula. Cardiac output was estimated by thermodilution. Measurements were made before and after intravenous injection of Meclofenamate, Parke Davis Ltd (4 mg/kg).3. Renal denervation caused a fall in renal cortical catecholamine concentration of approximately 50% by 48 hr.4. Resting renal blood flow did not differ significantly between denervated and innervated kidneys.5. Meclofenamate caused a significant rise in arterial pressure from a mean of 59 to 70 mmHg. In innervated kidneys, Meclofenamate caused a fall in renal blood flow from 8·1 ± 0·6 (mean ±
S.E. of mean) to 6·5 ± 0·4 ml./min.g kidney weight while in denervated kidneys it caused a fall from 8·9 ± 0·7 to 6·25 ± 0·3 ml./min.g.After Meclofenamate flow was redistributed away from the inner cortex in the innervated kidney and paradoxically towards the inner cortex in the denervated one.6. It was concluded that in conscious animals, resting sympathetic tone has little effect on renal blood flow. The exaggerated reduction in flow in the outer cortex of the denervated kidney following Meclofenamate may indicate denervation hypersensitivity to circulating catecholamines unmasked by reduced synthesis of vasodilator prostaglandins. Alternatively, renal sympathetic nerves may normally prime prostaglandin synthesis in the outer cortex.
The effect of diet on tissue levels of kinin‐forming enzyme in blood‐free rat gastro‐intestinal tract
Authors: Frankish N. H. , Zeitlin I. J. 
Published: December 2014

1. Kallikreins, kinin‐forming enzymes, are present in the wall of the gastro‐intestinal tract. The role of the kinin‐forming system in the gut is unknown. In the present study, a modified bio‐assay technique was used to detect the presence of tissue concentration gradients of kinin‐forming enzyme (KFE) at different levels of the rat gastro‐intestinal tract and the effect on them of diet.2. Segments of rat gut, perfused free of blood, were homogenized in 0·1
N‐HCl and activated by autolytic processes. Total KFE content was then determined by incubation of extract with standard kinin‐forming substrate, followed by bio‐assay of the released kinin using superfused oestrous rat uterus. Acid extraction of the KFE gave a recovery of 127·4% when compared with simple water extraction.3. Tissue concentrations of KFE were determined in stomach, duodenum, jejunum, terminal ileum, caecum and proximal and distal colon. Concentrations were determined after (A) normal diet, (B) water ad libitum for 24 hr and (C) isotonic glucose ad libitum for 60 hr.4. All the gut tissues contained KFE. After diet A there was least (19·5 ± 1·0 ng bradykinin equivalent formed per minute (KU) per gram wet weight) in the stomach and a single large peak (504 ± 92 KU .g−1 wet weight) in the caecum.5. The different dietary states produced changes only in the duodenum, the caecum and the distal colon. The duodenal level was raised when the organ was empty after diet B (140 ± 29 KU .g−1) and fell when filled with solid or fluid after diets A (57 ± 14 KU .g−1) and C (80 ± 17 KU .g−1) respectively. The caecal KFE level, which was high when the lumen was full after diet A, fell progressively as it was increasingly emptied after diets B (213 ± 41 KU .g−1) and C (105 ± 42 KU .g−1) respectively. The KFE concentration in the distal colon was low when the lumen was full after diets A (58 ± 10 KU .g−1) and B (66 ± 17 KU .g−1) and rose when the lumen was nearly empty after diet C (118 ± 17 KU .g−1).6. Kinin‐forming activity in rat intestinal extracts had a pH optimum at pH 8·5 and formed a bradykinin‐like spasmogen. The increased activity in the fasted rat duodenum was not significantly inhibited by soybean trypsin inhibitor (100 μg/ml.) while that in caeci from fed rats was inhibited by 17% (P < 0·05).7. These changes may indicate physiological involvement of the kallikrein‐kinin system in these organs.
Feeding in sheep during intraportal infusions of short‐chain fatty acids and the effect of liver denervation
Authors: Anil M. H. , Forbes J. M. 
Published: December 2014

1. Castrated male sheep were prepared with cannulae in the hepatic portal vein and jugular vein through which infusions lasting for 3 hr were made. Animals had free access to a pelleted feed the weight of which was continuously recorded so that feeding behaviour could be studied.2. Infusion into the portal vein of a mixture of salts of short‐chain fatty acids (acetate, propionate, butyrate: 55, 30, 15) caused a dose‐dependent depression in food intake, feeding stopping completely with 4·0 m‐mole/min of the mixture. Jugular infusion depressed intake slightly, compared with controls.3. Separate infusions of salts of the three acids showed that the effect of the mixture was due almost entirely to its propionate content; 1·2 m‐mole/min of propionate into the portal vein almost completely prevented feeding (39 g eaten per 3 hr) compared with jugular infusion at the same rate (210 g) or no infusion (205 g).4. Surgical sectioning of the hepatic nerve plexus around the wall of the hepatic artery was attempted. Of seven animals which recovered normal food intake, three continued to eat during portal vein infusions of propionate at 1·2 m‐mole/min; these sheep were subsequently shown to have been at least 95% denervated. One animal was 50% denervated and ate normally during some infusions but not others. In the remaining three, feeding was suppressed by portal vein infusion of propionate, and these were less than 75% denervated.5. It was concluded that there are receptors in the liver which are sensitive to propionate and which have afferent fibres in the hepatic plexus.
Haemodynamic responses to stimulation of the cardiac autonomic nerves in the anaesthetized cat with closed chest
Authors: Barnes R. J. , Bower E. A. , Rink T. J. 
Published: December 2014

1. The changes in cardiac output and mean right atrial pressure (R.A.P.) evoked by stimulation of the cardiac autonomic nerves were investigated in cats under chloralose anaesthesia, with unopened chests and spontaneous respiration, and with active vascular reflexes. Cardiac output was measured by thermal dilution; the technique used was calibrated against the direct Fick method.2. The initial values of R.A.P. and output were varied by infusion of dextran‐saline solution followed by withdrawal of blood. At positive values of R.A.P. withdrawal of blood caused a fall in R.A.P. with no change in cardiac output. At negative R.A.P. blood withdrawal caused a fall in output with little change in R.A.P.: the linear regression coefficient for output on R.A.P. was 48·2 ml./min.kg.mmHg (
S.E. 2·06, n = 63, nine cats).3. Stimulation of the right cardiac sympathetic nerve increased heart rate by 69·2 beats/min (
S.E. 4·0) from the resting rate of 158 beats/min (
S.E. 6·3, ten cats). The acceleration was accompanied in most instances by a rise in cardiac output and a fall in R.A.P. and the magnitude of the rise in output was related to that of the fall in R.A.P.4. In no experiment could R.A.P. be reduced below ‐2·5 mmHg either by withdrawal of blood or by sympathetic stimulation. At negative values of R.A.P. the fall in R.A.P. and rise in output evoked by sympathetic stimulation were small; substantial changes could be obtained only from positive initial values of R.A.P. The proportional increase in output evoked by a given proportional increase in heart rate during near‐maximal sympathetic stimulation had a linear relationship to the initial value of R.A.P. over the range ‐2 to +8 mmHg. The output increment was less than proportional to the rate increment at all values of R.A.P. below +3 mmHg.5. In five experiments stimulation of the left cardiac sympathetic nerve evoked a greater increase in output for a given increase in heart rate than did stimulation of the right nerve; on the other hand both nerves gave similar increments of output for a given fall in R.A.P.6. Stimulation of the distal end of the right vagus nerve slowed the heart and caused a fall in cardiac output and a rise in R.A.P. The change in output associated with a given change in R.A.P. was significantly greater (P = 0·05) during sympathetic than during vagal stimulation in 14 out of 18 tests; the difference increased as circulating volume was reduced.7. It is concluded that the relationship between cardiac output and R.A.P. during sympathetic and vagal stimulation is consistent with the hypothesis that neurally evoked changes in cardiac performance vary output mainly, but not exclusively, by inducing changes in R.A.P. which alter the pressure gradient for the return of blood to the right atrium from the periphery.
A comparison of effects evoked in guinea‐pig taenia caecum by purine nucleotides and by ‘purinergic’ nerve stimulation
Authors: Jager L. P. , Schevers J. A. M. 
Published: December 2014

1. Effects of adenosine and the adenosine nucleotides (ATP, ADP, AMP and CoA) on the guinea‐pig taenia caecum were studied by measuring simultaneously the changes in membrane potential and in contractility induced by these agents using the sucrose‐gap technique.2. In the presence of carbachol (5 × 10−8
M) the hyperpolarization and the relaxation induced by these agents was found to be closely correlated. Their different potencies suggested an action on the P2 type purinoceptor: ATP ≥ ADP ≥ AMP > CoA > AD.3. The transmitter released endogenously in the presence of carbachol (5 × 10−8
M) by the non‐adrenergic inhibitory (n.a.i.) nerves after half‐maximal stimulation induced an inhibitory junction potential (i.j.p.) which transiently counteracted the carbachol‐induced depolarization. This i.j.p. was mimicked by ATP, ADP, and AMP applied exogenously in concentrations of about 3 × 10−5
M, by CoA (3 × 10−4
M) and by adenosine (3 × 10−3
M).4. The results presented are in agreement with the hypothesis that the transmitter substance released by the n.a.i. nerves is a purine nucleotide, which in the guinea‐pig taenia caecum affects the smooth muscle cell membrane via the P2‐purinoceptor. Of the putative transmitters studied, ATP, ADP and AMP seem the most likely.
Importance of the kidneys for gastrin elimination and gastric function
Authors: El Munshid H. A. , Håkanson R. , Liedberg G. , Rehfeld J. F. , Sundler F. 
Published: December 2014

1. The gastrin concentrations in serum were elevated after nephrectomy in rats and mice indicating the importance of the kidney for elimination of gastrin in these species. In guinea‐pigs and rabbits nephrectomy did not cause increased serum gastrin concentrations. In rats there was a gradual rise in the serum gastrin level up to 48 hr after bilateral nephrectomy and also after ureteral ligation. After the latter operation the concentrations of gastrin in serum were lower than after nephrectomy. Significant elevation of the gastrin level 48 hr after ureteral ligation indicates that gastrin is eliminated at least partly through glomerular filtration. The gastric histidine decarboxylase activity after nephrectomy or ureteral ligation generally reflected the concentration of circulating gastrin.2. After bilateral ureteral ligation gastric acid secretion in conscious fistula rats was uniformly inhibited with no response to pentagastrin or histamine 24 or 48 hr after the operation. After nephrectomy basal acid secretion was reduced and there was no response to pentagastrin. The response to histamine was still present, although reduced at all dose levels. Linear transformation of the dose—response curve indicated mixed inhibition. The incidence of gastric ulcer was 75% 48 hr after nephrectomy and 30% after ureteral ligation. Since basal and pentagastrin‐stimulated acid secretion were unaffected by nephrectomy in rats with the upper two‐thirds of the intestine removed, the intestine appears to produce factors which are responsible for the inhibition of gastric secretion.2. On the whole, the gastrin concentration in serum and gastric histidine decarboxylase activity were not increased after five‐sixths nephrectomy. Gastric ulcers were seen in the rats with the highest serum urea levels; one in addition had high serum gastrin concentration and gastric histidine decarboxylase activity. Basal, pentagastrin‐ and histamine‐stimulated acid secretion were not affected by subtotal nephrectomy. It appears that in the rat about one sixth of the renal mass is the minimum required for handling gastrin degradation and excretion.
Force staircase kinetics in mammalian cardiac muscle: modulation by muscle length
Authors: Lakatta E. G. , Spurgeon H. A. 
Published: December 2014

1. Quiescent cat papillary muscles were stimulated to contract regularly at Lmax, the length at which force production is optimal, and at 0·85 Lmax. The resulting increase in force production (rate staircase) at each length was characterized as an exponential function.2. When stimulated from quiescence at 24 min−1 in a bathing fluid [Ca2+] of 2·5 m
M, sixteen of twenty‐three muscles exhibited biexponential increases in force production at both lengths. The coefficients of the exponential function at Lmax were 1·5‐2 times greater than their counterparts at the shorter length, and this length difference was highly significant. When the force staircases were normalized to the peak developed force attained at each length, the number of beats to attain 25, 50, 75, and 98% of peak force at 0·85 Lmax was approximately twice that required at Lmax.3. At a given length the force staircase (1) exhibited a dependency on the number of beats rather than on stimulation frequency over a range of 12‐60 min−1, (2) was accelerated by increasing the bathing fluid [Ca2+] from 1·0 to 5·0 m
M, (3) was accelerated in the presence of isoproterenol, and (4) was retarded in the presence of
DL‐verapamil. Over the entire range of bathing fluid [Ca2+] and at all stimulation frequencies 24 min−1 and above, more beats were required to complete a given level of the normalized staircase at 0·85 Lmax than at Lmax. There was no length difference in the presence of verapamil. These data suggest that transsarcolemmal Ca2+ influx is an important determinant of the kinetics of the force staircase, and the length dependence of the latter indicates that muscle length is an important determinant of transsarcolemmal Ca2+ influx.4. This conclusion was strengthened by the results of additional studies in which the [Ca2+] of the bathing fluid was abruptly increased from 1·0 to 5·0 m
M with the muscle beating in the steady state. The resulting increase in force production (Ca2+ staircase) was described by a monoexponential function with a greater coefficient at Lmax than 0·85 Lmax; when normalized to the peak force difference in the two [Ca2+] at each length, a given level of the staircase was achieved in significantly fewer beats at Lmax than at the shorter length.5. The data provide a mechanism which, in part, explains the length dependence of excitation‐contraction coupling in cardiac muscle with intact sarcolemmae.
Binding of scorpion toxin to sodium channels in vitro and its modification by β‐bungarotoxin
Authors: Okamoto Harumasa 
Published: December 2014

1. Binding of a purified scorpion toxin to membrane fragments isolated from electroplaque of an electric eel Electrophorus electricus was studied using a radio‐iodinated toxin.2. A scorpion toxin was purified from the venom of Leiurus quinquestriatus and iodinated with 125I in a lactoperoxidase‐catalysed reaction. Monoiodinated toxin, isolated by an ion exchange chromatography, retarded the inactivation kinetics of Na current to a similar extent as the native toxin, indicating that radioiodination did not appreciably affect physiological and binding properties of the native toxin.3. Analyses of binding properties by Scatchard plots showed the presence of two classes of binding sites (with low and high affinities) in the membrane preparation from eel electroplaque; similar preparation from an electric skate, of which the electroplaque is known to be devoid of Na channels, possessed only the low affinity sites.4. The number of high affinity sites in the eel preparation was 41·8 ± 10·5 p‐mole/g tissue; the value was within the range reported for tetrodotoxin binding to similar preparations (15‐148 p‐mole/g tissue).5. A variety of cations (Na+, Mn2+ and La3+) inhibited the high affinity scorpion toxin binding, as indicated for the toxin binding to Na channels by a previous electrophysiological study. KD value in the presence of 120 m
M‐Na+ (approx. 8 n
M) agreed reasonably with that (approx. 10n
M) reported for the scorpion toxin binding to excitable neuroblastoma cells or synaptic nerve ending particles under conditions where membrane potential was depolarized by the addition of 135 m
M‐KCl.6. Pretreatment of the eel membrane preparation with β‐bungarotoxin (7‐44 ng/ml.) in the presence of Ca ions (10‐200 μ
M) resulted in a substantial loss of high affinity binding of scorpion toxin. When phospholipase A2 activity of the β‐toxin was inactivated by a chemical modification with p‐bromophenacyl bromide, the inhibitory action of the β‐bungarotoxin was abolished.7. It is concluded that a high affinity binding of scorpion toxin to the eel electroplaque membrane fragments represents the binding to Na channels in vitro, and that phospholipase A2 activity of β‐bungarotoxin interferes with the binding of scorpion toxin to Na channels.
Temporal and spatial characteristics of the voltage response of rods in the retina of the snapping turtle
Authors: Detwiler P. B. , Hodgkin A. L. , McNaughton P. A. 
Published: December 2014

1. In response to strong, large‐field flashes the dark‐adapted rods of Chelydra serpentina gave initial hyperpolarizing responses of 30‐40 mV, declining rapidly to plateaus of 10‐15 mV which lasted 20 sec or more.2. In the most sensitive cells the flash‐sensitivity at 520 nm to a large illuminated area was 3‐6 mV per photoisomerization (assuming an effective collecting area of 13·6 μm2).3. The initial response to a step of light agreed with that predicted by super‐position from the flash response but even with very weak lights the step response fell below the predicted curve at times longer than about 2 sec.4. The step sensitivity defined from the initial peak of the response to a step of light was 2‐6 mV photoisomerization−1 sec, about 1000 times greater than the most sensitive cones in the turtle retina.5. The response to a small weakly illuminated spot (radius 21 μm) reached a peak later and lasted longer than the linear response to a weakly illuminated large area (radius 570 μm).6. The difference in sensitivity between large and small spots was reasonably consistent with the apparent space constant of the rod network obtained from the exponential decline of the flash response on either side of an illuminated strip.7. As others have found, strong flashes did not give an initial hyperpolarizing transient when the radius of the spot was less than about 50 μm.8. Experiments made by flashing long narrow strips of light onto the retina showed that the response spread a long way initially (λ ≑ 70 μm) and then contracted down to a relatively small region (λ ≑ 25 μm) at times of about 2 sec. When the line source was at some distance from the impaled rod the response reached a peak earlier and was shorter than when the source was close.9. The results in (8) can be explained quantitatively by assuming that delayed voltage‐dependent conductance changes mimic an inductance and make the rod network behave like a high‐pass filter with series resistance and parallel inductance.10. In sensitive rods, flash responses varied randomly with a variance which was about 1/30 of that expected in an isolated cell; this reduction in noise is satisfactorily explained by electrical coupling between rods.11. The variance peak usually occurred later than the potential peak of the rod response.12. The high‐pass filter characteristics of the rod‐network help to explain several puzzling features of the behaviour of rods, for example (1), (5), (7), (8) and (11) of this summary.13. The high‐pass filter characteristics of the rod‐network may help it to optimize the signal to noise ratio by integrating over a large area for rapid signals and over a small one for slow signals.
Origin of the humoral factor responsible for compensatory renal hypertrophy
Authors: Dicker S. E. , Morris Christine A. 
Published: December 2014

1. Rats were unilaterally nephrectomized and the remaining kidney was removed 10 min after the operation.2. Cortical slices from both kidneys were incubated in culture medium in the presence of freeze‐dried plasma from a control animal, for 4 hr. When renal cortical slices from a normal animal were now added to and incubated in the medium in which cortical slices from the remaining kidney (i.e. the kidney removed 10 min after unilateral nephrectomy) had been incubated, they showed an increase of protein content and dry weight. This increase did not occur when slices from normal kidneys were incubated in culture medium in which the first kidney had been incubated.3. The increase of protein content and dry weight of cortical slices from normal kidneys did not occur when incubated in culture medium in which cortical slices from the remaining kidney had been incubated when freeze‐dried plasma from normal rats had been substituted by freeze‐dried plasma from anephric rats.4. Since normal plasma which does not normally promote protein accretion in normal cortical slices in vitro can do so after it has been incubated with cortical slices from a kidney removed 10 min after unilateral nephrectomy, it is suggested that normal plasma contains a precursor of renal origin which is ‘activated’ when in the presence of a remaining kidney removed shortly after unilateral nephrectomy.