bluuebunny/crossref_metadata_2025_split huggingface dataset:
The influence of corticosteroids on the secretion of corticotrophin and its hypothalamic releasing hormone
Authors: Buckingham Julia C. 
Published: December 2014

1. The effects of stress, adrenalectomy and corticosterone treatment on the functional activity of the hypothalamo‐pituitary‐adrenocortical system have been studied using highly sensitive and precise bio‐assay methods for the determination of ACTH and CRH.2. Adrenalectomy resulted in a rise and corticosterone treatment a fall in the hypothalamic CRH content and the plasma ACTH concentration.3. Stress caused a fall followed by a rise in the hypothalamic CRH content, a rise in the pituitary and plasma ACTH concentrations and an increase in the plasma corticosterone concentration.4. The stress‐induced changes in hypothalamic CRH content and pituitary and plasma ACTH were exaggerated in adrenalectomized rats but normal in adrenalectomized rats treated with corticosterone. They were also normal in animals injected
I.P. with corticosterone 15 min before the stress but inhibited in those similarly treated 60 min previously.5. The ability of adenohypophyses and hypothalami to synthesize and release in vitro ACTH and CRH respectively in response to trophic stimuli was exaggerated in glands removed from adrenalectomized rats and reduced in those removed from corticosterone‐treated rats.6. Addition of corticosterone to the pre‐incubation medium reduced the capacities of adenohypophyses and hypothalami removed from untreated rats to synthesize and release ACTH and CRH respectively.
The transport of the lead cation across the intestinal membrane
Authors: Blair J. A. , Coleman I. P. L. , Hilburn M. E. 
Published: December 2014

1. The transport of the lead cation has been investigated using the everted sac preparation of Wilson & Wiseman (1954).2. Only a small percentage of lead was transported into the serosal compartment but there was a rapid and massive uptake onto the tissue. There was no significant difference in the amount of lead cations transported across different regions of the small intestine.3. Both the rate of transport into the serosal compartment and the tissue uptake increased linearly with increasing concentration of the lead cation, from 10−7
M to 5 × 10−5
M. Little evidence for saturation of serosal transport or tissue uptake was found.4. Lead transport into the serosal compartment appeared to be related to water movement, but was little affected by changes in glucose concentration and temperature.5. It is concluded that lead is transported into the serosal space by a process of passive diffusion linked to water transport.6. The interaction between lead ions and the intestinal tissue was extremely tenacious and displayed characteristics of covalent bonding.7. It is suggested that the lead cation interacts with tissue phosphate ions thus removing lead ions from the transport pool. Chelation of lead to form a neutral species reduces this interaction and also promotes transport.
Non‐electrolyte permeability of trout gills: effect of temperature and adrenaline
Authors: Isaia J. 
Published: December 2014

1. The gill permeability to various non‐electrolytes (Ps) was measured in fresh‐water and sea‐water adapted trout (Salmo gairdneri). This study was performed in vitro using a ‘head‐perfused’ preparation. The influence of temperature and adrenaline (10−6
M) on permeability to non‐electrolytes was also investigated.2. During salt adaptation Pbutanol and Pwater decrease, Pmannitol rises and Pdextran stays constant. In view of recently acquired morphological data these results back up the hypothesis of different pathways across the gill epithelium (transcellular, vesicular and paracellular) according to the physico‐chemical characteristics of the molecules. The low selectivity of the gill epithelium as a function of the liposolubility of the molecules used testifies to the hydrophilic nature of diffusion across this epithelium, a feature becoming more pronounced during salt adaptation.3. The activation energies are about 4 kcal/mol, an energy comparable to diffusion in water for most of the substances tested, exceptions being butanol for fresh‐water adapted gills and water for fresh‐water and sea‐water adapted gills. Arrhenius plots for butanol in fresh water gills show a transition temperature at 15 °C, suggesting an increased membrane lipid fluidity above this temperature.4. Adrenaline has no effect on Pmannitol and Pdextran, but increases Pbutanol and Pwater selectively according to the adaptation medium (+ 160% and + 100% in fresh water and + 25% and + 20% in sea water respectively). These results point to an effect of this catecholamine on the membrane lipid fluidity.
Dark‐adaptation of the aspartate‐isolated rod receptor potential of the frog retina: threshold measurements
Authors: Donner K. O. , Hemilä S. O. 
Published: December 2014

1. The dark‐adaptation of the aspartate‐isolated rod receptor potential of the isolated and perfused frog retina has been measured after bleaching about 5‐10% of the rhodopsin. The fraction bleached (ΔR) and the decay of rhodopsin photoproducts were determined using alternating measurements with a photometric technique (Donner & Hemilä, 1975).2. The dark‐adaptation time course of the log threshold elevation is exponential, log It/I0 = W exp (‐t/τ)+P, where W is the extrapolated value for log It/I0‐P at t = 0 and P is log It/I0 for t = ∞. When ΔR increases from 2 to 10% W increases from ca. 2·6 to ca. 5. The time constant τ is about 13 min at 9 °C and 7 min at 14 °C (ΔR = 5‐10%).3. When the bleaching period is extended, keeping the amount bleached (I×t) constant, dark‐adaptation is completed earlier.4. The time course of dark‐adaptation and the decay of the photoproduct ‘retinal’ are similar, as is also their dependence on temperature (Q10 ≈ 3).5. The permanent log threshold rise P is approximately proportional to ΔR after small bleaches; when more than about 10% is bleached the slope of the curve P(ΔR) decreases. P is considerably larger (about 2·5‐fold) for the same fraction bleached in experiments at 14 °C as compared to experiments at 9 °C.6. A comparison with previously obtained corresponding values for dark‐adaptation after small bleaches at the ganglion cell level shows a close agreement between the time constants for the dark‐adaptation curve, its range and the dependence of threshold on the fraction of rhodopsin bleached.
Phosphate efflux and oxygen consumption in small non‐myelinated nerve fibres at rest and during activity
Authors: Ritchie J. M. , Straub R. W. 
Published: December 2014

1. The oxygen consumption and the movements of labelled phosphate were measured in garfish olfactory nerve at rest and during activity.2. In solutions with 2·5 m
M‐K and 0·2 m
M‐phosphate the resting oxygen consumption was 0·206 m‐mole/kg.min; activity at 2 sec−1 produced an extra oxygen consumption of 2·46 μmole/kg.impulse. The extra oxygen consumption declined exponentially with a time constant of 2·62 min at 22‐26 °C.3. The phosphate efflux, measured simultaneously, had a resting efflux rate constant of 1·24 × 10−3 min−1; activity at 2 sec−1 produced an extra fractional loss of 9·38 × 10−6 impulse−1. The increase in phosphate efflux followed almost the same time course as the increase in oxygen consumption.4. Increasing the frequency of stimulation from 2 sec−1 to 3 or 5 sec−1 decreased both the extra oxygen consumption and the extra fractional loss of phosphate. When the frequency was decreased to 0·5 or 1 sec−1 the extra oxygen consumption per impulse increased, while the extra phosphate liberation was lowered.5. Changing the phosphate concentration did not much affect the extra oxygen consumption; on the other hand, lowering or increasing the phosphate from the standard 0.2 m
M decreased both the resting and the stimulated phosphate efflux.6. Lowering the K from the standard 2·5 m
M did not affect the extra oxygen consumption, but increased both the resting and the extra loss of phosphate. At higher K concentrations the extra oxygen consumption and the extra fractional loss of phosphate decreased without much change in the resting phosphate efflux.7. Application of 1‐20 μ
M‐strophanthidin produced a transient decrease in the resting phosphate efflux without much change in resting oxygen consumption. With 10 or 20 μ
M‐strophanthidin the extra fractional loss of phosphate and the extra oxygen consumption were both lowered in approximately the same proportions.8. The findings are consistent with the hypothesis that the increase in intracellular inorganic phosphate that results from increased break‐down of ATP after activity, is the main cause for the increased phosphate efflux. A fraction of the increase in intracellular phosphate only appears to be liberated to the outside, the value of the fraction depending on the resting phosphate efflux before activity.9. The initial increase in intracellular inorganic phosphate after an impulse, estimated from the oxygen consumption or the phosphate fluxes, appears to be about 12‐19 μmole/kg nerve, remarkably close to the value known from chemical analysis.
The effect of pentagastrin on peptic secretion in man
Authors: Braganza Joan M. , Herman K. , Hine Pauline , Kay G. 
Published: December 2014

1. We have studied the peptic responses of the intact human stomach to stimulation by doses of pentagastrin which elicit a maximal acid response.2. In twelve patients an intramuscular injection of pentagastrin (6 μg/kg) was followed by a prompt increase in acid output which attained a peak value eight times higher than the basal value in the period 15‐30 min after stimulation. The pattern of the peptic response was similar, but the peak output of pepsin was only three times the output in unstimulated juice.3. In ten subjects the acid and peptic responses to
I.V. infusion of pentagastrin (1·2 μg/kg per hr) were studied using a gastric perfusion technique with 14C‐labelled polyethylene glycol as non‐absorbable marker. In seven of these ten subjects the pH of duodenal contents exceeded 6, and less than 0·5 m‐mole HCl per 15 min entered the duodenum throughout the tests. In this subgroup pentagastrin evoked a strong acid response but no peptic response.4. In three subjects the pH of duodenal juice was less than 5·5 at times when more than 1 m‐mole HCl per 15 min entered the duodenum. The acid response to pentagastrin differed considerably in the three subjects, but in each individual the output of pepsin increased each time an excess of HCl entered the duodenum.5. Since pentagastrin infused in a dose which maximally stimulates acid did not significantly increase the output of pepsin provided no HCl entered the duodenum we conclude that pentagastrin does not stimulate the secretion of pepsin in man. The transient insignificant peptic response to pentagastrin infusions, and the small but significant response to bolus injections of pentagastrin, can be explained as a wash‐out phenomenon.
Hypothalamic receptors influencing the secretion of corticotrophin releasing hormone in the rat
Authors: Buckingham Julia C. , Hodges J. R. 
Published: December 2014

1. The production of corticotrophin releasing hormone (CRH) by the rat hypothalamus in vitro was studied in the presence and absence of various neurotransmitter substances and drugs which mimic or antagonize their actions.2. Acetylcholine, nicotine and bethanechol increased, in a dose‐related manner, hypothalamic CRH release and content but the maximal responses to bethanechol or nicotine were less than those to acetylcholine.3. The actions of acetylcholine were antagonized by atropine, pempidine and hexamethonium but were completely inhibited only when atropine and pempidine were given together. The effects of nicotine were abolished by pempidine but not by atropine while those of bethanechol were abolished by atropine but not by pempidine.4. Acetylcholine‐induced hypothalamic CRH activity was also antagonized by cyproheptadine but not by methysergide.5. 5‐Hydroxytryptamine caused dose‐related increases in hypothalamic CRH release and content. Its effects were antagonized by cyproheptadine and methysergide but not by atropine, pempidine or hexamethonium.6. Acetylcholine‐induced increases in hypothalamic CRH production were reduced by GABA, noradrenaline, adrenaline, methoxamine and phenylephrine but not by isoprenaline. The actions of GABA were antagonized by bicuculline and those of noradrenaline by phentolamine but not by atenolol.7. The results suggest the presence of nicotinic and muscarinic cholinoceptors, 5‐hydroxytryptamine receptors, α‐adrenoceptors and GABA‐receptors within the hypothalamus all of which may be important in the control of CRH secretion.
The role of circulating renin in drinking in response to isoprenaline
Authors: Atkinson J. , Kaesermann H.‐P. , Lambelet Josette , Peters G. , Peters‐Haefeli Lise 
Published: December 2014

1. In nephrectomized rats,
S.C. (0·12 mg. kg body wt.−1) or intracerebroventricular (
I.C.V.: 0·03 mg. kg−1), isoprenaline failed to elicit drinking. However, when preceded (5‐20 min) by a non‐dipsogenic dose of
I.V. pig renin,
S.C. isoprenaline induced a marked, and
I.C.V. isoprenaline a smaller drinking response. 2 hr after
I.V. renin,
S.C. isoprenaline no longer caused drinking.2. Pig renin did not enhance drinking in response to 0·12 mg. kg−1 isoprenaline
S.C. in intact or sham‐operated rats.3. Isoprenaline (0·12 mg. kg body wt.−1,
S.C.) caused a larger fall of blood pressure in unanaesthetized nephrectomized than in intact unanaesthetized rats, but it was not the resulting hypotension that interfered with the nephrectomized rats’ ability to drink, since intact rats with similar falls in blood pressure drank avidly in response to large doses of isoprenaline.4. Since the rate of inactivation of pig renin in nephrectomized rats was not modified by isoprenaline, drinking in nephrectomized animals in response to renin+isoprenaline was not attributable to increased plasma renin levels.5. Since isoprenaline induces drinking in the presence of circulating renin, but in the absence of renin release from kidneys, renin plays a permissive role in isoprenaline‐induced drinking. Angiotensin and isoprenaline may interact at the level of intracranial receptors.
Neural connexions between the medial forebrain bundle, the preoptic area and the basal hypothalamus in the rat: an electrophysiological study
Authors: Perkins M. N. , Whitehead Saffron A. 
Published: December 2014

1. Electrophysiological experiments have been performed on intact cycling female rats to investigate the neural connexions that exist between the medial forebrain bundle, the anterior hypothalamic region, which included the preoptic area, and the basal hypothalamus. Recordings have been made from a total of 351 neurones in the anterior hypothalamus of which 216 were responsive to stimulation of either or both the medial forebrain bundle and basal hypothalamus (arcuate and ventromedial nuclei).2. Forty‐six of these cells were responsive to a stimulus applied both to the medial forebrain bundle and the basal hypothalamus with a variety of response combinations. The majority of neurones were orthodromically activated by stimulation in both sites. Inhibition by stimulation of the medial forebrain bundle coupled with orthodromic excitation from the basal hypothalamus, or the reverse situation, was also encountered frequently.3. A few cells were antidromically invaded by the stimulation of the medial forebrain bundle and these received orthodromic or inhibitory inputs from the basal hypothalamus, although one unit outside the anterior hypothalamus was antidromically activated by both stimuli.4. Ninety per cent of all the doubly responsive units that could be antidromically activated by stimulation of the basal hypothalamus received an orthodromic input from the medial forebrain bundle, and no cells in the anterior hypothalamus that projected to the basal hypothalamus were found to receive an inhibitory input from the medial forebrain bundle.5. These results provide electrophysiological evidence for inhibitory and excitatory inputs from the medial forebrain bundle to the preoptic and anterior hypothalamic cells that either project to, or receive connexions from, the basal hypothalamus. Neurones in the preoptic area which project to the basal hypothalamus are implicated in the control of anterior pituitary function, particularly gonadotrophin secretion. These experiments, coupled with functional studies, suggest that there is an excitatory input from the medial forebrain bundle to these preoptic and anterior hypothalamic cells which may modulate adenohypophyseal secretions.
Effects of atropine on secretion and motility in isolated gastric mucosa and attached muscularis externa from ferret and cat
Authors: Roth S. H. , Schofield B. , Yates J. C. 
Published: December 2014

1. A combined in vitro preparation of gastric mucosa and adjacent muscle from young ferrets and kittens has been used to study the effects of atropine on acid secretion and motility produced by acetylcholine (ACh) and pentagastrin.2. The minimal dose of atropine required to abolish a maximum secretory response to ACh also prevented the associated motility response. This dose of atropine also blocked the motility response to pentagastrin, but was without influence on the secretory effect of this agent. A 103 times larger dose of atropine reduced the secretory effect of pentagastrin by half, probably not by anti‐muscarinic effect. The results exclude the possibility that the acid secretory response to pentagastrin necessarily involves a cholinergic receptor.3. The results support the view that the response of the fundic smooth muscle to pentagastrin depends on the excitation of cholinergic nerves.4. No evidence has been found of any cholinergic component in the acid secretory response to pentagastrin. In assessing the significance of this result, however, it must be remembered that the Auerbach plexus has been removed over the major part of the mucosa, and the Meissner plexus deprived of input and probably damaged.5. The results are compatible with the hypothesis that the depressant effect of atropine on acid secretion produced by gastrin and its derivatives is due to the elimination of a cholinergic potentiating influence arising in the intramural plexuses. The residual Meissner plexus elements in this in vitro preparation appear inadequate to sustain this effect.
Influence of potassium, sodium, perfusion pressure, and isoprenaline on renin release induced by acute calcium deprivation
Authors: Fray John C. S. , Park C. S. 
Published: December 2014

1. These studies were conducted in isolated perfused rat kidneys to determine the influence of perfusion pressure, isoprenaline, K, and Na on renin release stimulated by acute Ca deprivation.2. Removing Ca from the perfusion medium for 10 min stimulated renin release and reintroducing Ca returned it toward control values.3. Lowering concentration of Ca in the perfusion medium from 5 to 0 m
M increased the effectiveness of low perfusion pressure (50 mmHg) and isoprenaline (2·43 μ
M) in stimulating renin release.4. At higher perfusion pressure (150 mmHg), renin release was inhibited in perfusion medium containing 2·5 m
M‐Ca but not in medium containing no Ca. In fact, high perfusion pressure stimulated renin release when the perfusion medium was without Ca.5. Raising concentration of K in the perfusion medium partially inhibited the renin release induced by Ca deprivation. Adding 5 m
M‐EGTA to Ca‐deprived medium stimulated a greater rate of renin release than that of Ca‐deprived medium alone. This greater renin release was also partially inhibited by raising K concentration in the perfusion medium.6. Lowering concentration of Na in the perfusion medium from 145 to 25 m
M partially inhibited the renin release induced by Ca deprivation in the presence of low perfusion pressure or isoprenaline.7. These findings support the hypothesis that a decreased concentration of Ca in the cytoplasm of the juxtaglomerular cell stimulates renin release and increased Ca inhibits renin release. The sequence of events which leads to changes in cytoplasmic Ca might depend on the concentration of Ca in the perfusion medium, the renal perfusion pressure, the membrane potential of the juxtaglomerular cells, and Ca—Na exchange mechanisms.
Electrophysiology and pharmacology of striated muscle fibres cultured from dissociated neonatal rat pineal glands
Authors: Freschi J. E. , Parfitt A. G. , Shain W. G. 
Published: December 2014

1. Striated muscle fibres were found in each of twenty consecutive pineal glands cultured from individual neonatal rats.2. In subsequent experiments performed with dissociated cultures of pineal organs pooled from several litters, myotubes were first visible after about 1 week in culture.3. During the next several weeks the myotubes increased in size, developed crossstriations, and began to twitch spontaneously.4. The resting membrane potential increased with age in culture. All myotubes studied showed delayed rectification. Action potentials either occurred spontaneously or could be evoked if the membrane were sufficiently polarized. No spontaneous end plate potentials were seen.5. Acetylcholine (ACh) produced a brief, monophasic depolarizing response. Noradrenaline, serotonin, melatonin, dopamine, and γ‐aminobutyric acid (GABA) had no effect on the resting membrane potential when applied iontophoretically.6. The ACh response was reversibly blocked by 10−6
M‐tubocurarine and irreversibly blocked by 10−6
M‐α‐bungarotoxin. Atropine (10−4
M) reduced the amplitude and shortened the time course of the ACh response, and 10−3
M‐atropine produced complete but reversible inhibition.7. We conclude that pineal muscle fibres are electrophysiologically and pharmacologically similar to skeletal muscle fibres in vitro. Although the pineal gland has undetectable levels of ACh, pineal muscle develops ACh receptors but not noradrenaline, serotonin, melatonin, dopamine, or GABA receptors mediating electrophysiological responses, although these latter substances (except dopamine) are found in the pineal.
Drinking behaviour in rats treated with isoprenaline, angiotensin II or angiotensin antagonists
Authors: Chiaraviglio Emma 
Published: December 2014

1. Isoprenaline hydrochloride injected subcutaneously in rats given a choice test of 1·8% NaCl and water, first induced saline intake which started immediately and was almost concluded in 15 min, followed by a copious water intake. When either saline or water were given in a separate test, saline intake surpassed the water intake in the first 15 min.2. The delay of 15, 30 or 60 min after injection of isoprenaline, 100 μg/kg, before drinking was allowed, significantly reduced saline intake but did not modify the amount of water subsequently drunk.3. Isoprenaline caused a sudden drop in arterial blood pressure, the extent and duration depending on the dose. The time of maximum drop 3‐4 min after injection coincided with the time the rat drank salt.4. Isoprenaline‐induced saline drinking was significantly reduced after bilateral nephrectomy but water intake was unaffected.5. The beta‐adrenoceptor blocking agent, propranolol, inhibited isoprenaline‐induced NaCl and water intake, while the alpha‐adrenoceptor antagonist phenoxybenzamine abolished isoprenaline‐induced NaCl intake and enhanced water intake.6. Saralasin acetate (P‐113), a competitive inhibitor of angiotensin II, given into the third brain ventricle, prevented the isoprenaline‐induced NaCl and water intake as well as angiotensin II‐induced drinking. The angiotensin converting enzyme inhibitor SQ‐20881 reduced the isoprenaline‐induced NaCl and water intake.7. In conclusion, hypotension might be a component of salt drinking evoked by isoprenaline although the dipsogenic action of beta‐stimulation is mainly due to endogenous renin‐angiotensin activation.