bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF α‐ADRENOCEPTOR ANTAGONISTS ON CONTRACTILE RESPONSES TO 5‐HYDROXYTRYPTAMINE IN DOG SAPHENOUS VEIN
Authors: HUMPHREY P. P. A. 
Published: July 2012

5‐Hydroxytryptamine (5‐HT) contracted isolated saphenous vein strips of the dog, producing a biphasic concentration‐effect curve. The first phase occurred with low concentrations of 5‐HT (1.0 × 10−8 to 5.0 × 10−6mol/1) with a plateau between 1.0 × 10−6mol/1 and 1.0 × 10−5mol/1. The second phase occurred with high concentrations of 5‐HT (greater than 1.0 × 10−5 mol/1).
The α‐adrenoceptor antagonists, phentolamine (5.0 × 10−8 to 5.0 × 10−7 mol/1), labetalol (1.0 × 10−6 to 1.0 × 10−5 mol/1) and thymoxamine (1.0 × 10−6 to 1.0 × 10−5 mol/1), antagonized responses to high concentrations of 5‐HT but responses to low concentrations of 5‐HT were not antagonized.
The effects of high concentrations of 5‐HT were antagonized by cocaine (1.0 × 10−6 to 1.0 × 10−5 mol/1) and were not evident in veins removed from dogs pretreated with syrosingopine.
It is concluded that in the saphenous vein, low concentrations of 5‐HT act directly on specific 5‐HT receptors and that high concentrations of 5‐HT also act indirectly on α‐adrenoceptors by displacing noradrenaline from neuronal stores.
ANTIDIURETIC EFFECT OF MORPHINE IN THE RAT: TOLERANCE AND PHYSICAL DEPENDENCE
Authors: HUIDOBRO F. 
Published: July 2012

Injection of rats with morphine or methadone, before they received a water load equivalent to 5% of their body weight, produced a dose‐dependent antidiuretic effect. Following the antidiuresis, urine was eliminated with kinetics similar to control untreated rats.
The antidiuretic effect of morphine or methadone was blocked by naloxone administered before the opiate, or reversed when given after the opiate.
Rats implanted with morphine pellets developed a marked degree of tolerance to the antidiuretic effect of morphine. Tolerance was also obtained on injection of three daily doses of morphine or methadone over two days.
Withdrawal symptoms were precipitated by naloxone in rats implanted with pellets of morphine; under these conditions the animals showed a marked reduction in urine production as compared to naive rats.
AGE‐RELATED CHANGES IN THE RESPONSE OF RABBIT ISOLATED AORTAE TO VASOACTIVE AGENTS
Authors: HAYASHI SHIGEHIRO , TODA NOBORU 
Published: July 2012

In helically‐cut strips of aortae from rabbits of different ages (2 to 360 days old), responses to vasoconstrictor and vasodilator agents were compared.
The passive tension developed by the same magnitude of stretch was markedly less in aortae from immature rabbits than in aortae from mature rabbits.
Contractile responses to noradrenaline and K+ increased with age in the range from 2 to 90 days. High concentrations of noradrenaline (10−5 and 5 × 10−5m) produced relaxation of aortic strips from immature rabbits (2 to 30 days). The response to histamine was not altered with age. Age‐dependent reductions (90 to 360 days) in the response to 5‐hydroxytryptamine were observed.
Relaxations induced by isoprenaline of aortic strips contracted with prostaglandin F2at increased with age in the range from 2 to 30 days but decreased with age from 30 to 360 days. Similar age‐related alterations in the relaxant response to adenosine were observed.
It is concluded that aortae from immature rabbits are more distensible than those from mature rabbits; α‐adrenoceptors mature during an early postnatal period (2 to 30 days), and 5‐hydroxytryptamine receptor mechanisms deteriorate with age (older than 90 days). The β‐receptor mechanism does not seem to alter greatly with age.
THE INFLUENCE OF SODIUM AND POTASSIUM SUPPLEMENTS ON THE DIURETIC RESPONSES TO FRUSEMIDE ADMINISTRATION IN NORMAL SUBJECTS
Authors: BRANCH ROBERT A. , COLE EDWARD , HORTH CHARLES E. , JACKSON LYNNE , RAMSAY LARRY E. , SHELTON JOHN 
Published: July 2012

Twelve normal subjects received (1) normal diet, (2) normal diet with 100 mmol supplementary sodium chloride and (3) normal diet with 96 mmol supplementary potassium chloride, each for 10 days, in a balanced cross‐over study according to a Latin Square design. At the end of each study period, the subjects received 80 mg frusemide orally. Each study period was separated from the other by 10 days.
Changes in urinary electrolyte excretion occurred within the first four days of each dietary period then remained constant, with significant differences in urinary Na/K ratio between the dietary regimes.
Between‐subject correlations, using the mean values over the three study periods, demonstrated significant associations between plasma uric acid and urinary Na/K ratio and between plasma prolactin and urinary potassium excretion.
Urinary potassium excretion and Na/K ratio following frusemide were influenced significantly by alteration of diet but there was no change in sodium excretion.
Between‐subject correlations of pretreatment variables with diuretic response, using the mean values over the three study periods, demonstrated significant associations between both pretreatment urinary Na/K ratio and plasma uric acid and respectively the urinary potassium excretion and urinary Na/K ratio in response to frusemide.
While the response to frusemide was altered by short‐term changes in dietary sodium and potassium, the difference was less than expected from observations in two populations with customary diets differing in similar manner.
EFFECTS OF SOMATOSTATIN ON GASTRIC ACID SECRETION AND ON LIPID AND CARBOHYDRATE METABOLISM IN THE RAT
Authors: LINSCHEER WILLEM G. , RAHEJA KRISHAN L. 
Published: July 2012

Studies were conducted to examine the effects of somatostatin on pentagastrin‐induced gastric acid secretion, and on bile, plasma and liver lipid composition in the rat.
In addition, liver glycogen and plasma glucose concentrations were measured.
Somatostatin was administered intravenously as a bolus (100 ug) at the start of the experiment followed by a continuous infusion (50 ug/h) for 2 h.
Controls were infused with isotonic saline (1 ml/h) throughout the experiment. Gastric secretions and bile were collected during the infusions.
Somatostatin significantly decreased the volume of gastric secretion as well as total gastric acid output but it had no effect on bile flow or bile lipid composition.
Plasma and liver lipids were not affected. Plasma glucose concentrations were significantly elevated but liver glycogen was not changed.
Our results suggest that somatostatin probably decreases glucose uptake by peripheral tissue. The effect of somatostatin on bile composition and glucose levels in the rat is different from observations reported in other species.
ROLE OF 5‐HYDROXYTRYPTAMINE IN THE VASOCONSTRICTOR ACTION OF COMPOUND 48/80 IN THE RAT FEMORAL VASCULATURE
Authors: SAKAI K. 
Published: July 2012

The effect of compound 48/80 on the rat femoral vasculature was examined by means of a cross‐circulation technique.
Intra‐arterial injection of increasing doses (1.5 to 15 ug) of compound 48/80 caused dose‐dependent vasoconstriction preceded by transient vasodilatation. The vasoconstriction was significantly reduced in reserpine‐treated preparations and converted to vasodilatation by methysergide.
When the vasoconstrictor response to a large dose (300 ug) of adenosine was abolished by repeated administration, the response to compound 48/80 remained unaltered.
The present results indicate that the femoral arterial vasoconstriction by compound 48/80 in the rat is mediated by the release of 5‐hydroxytryptamine (5‐HT); this 5‐HT may be liberated from a different storage site from that released by adenosine.
HYPERPOLARIZING ‘α2’‐ADRENOCEPTORS IN RAT SYMPATHETIC GANGLIA
Authors: BROWN D.A. , CAULFIELD M.P. 
Published: July 2012

Receptors mediating catecholamine‐induced hyperpolarization of isolated superior cervical sympathetic ganglia of the rat have been characterized by means of an extracellular recording method.
(—)‐Noradrenaline (EC50, 1.7 ± 0.6 μm) produced an immediate low‐amplitude (<400 uV) hyperpolarization. The hyperpolarization was increased on removal of external Ca2+ or on reduction of external K+ from 6 to 2 mm. Hyperpolarization was unaffected by changing the temperature from 25° to 37°C.
Hyperpolarization was also produced by the following agonists (potencies relative to (—)‐noradrenaline): (—)‐noradrenaline 1; (±)‐isoprenaline 0.41; (—)‐phenylephrine 0.40; (+)‐noradrenaline 0.13; 2‐amino‐6,7‐dihydroxy tetrahydronaphthalene (ADTN) 0.25; dopamine 0.1; methoxamine 0.012; amidephrine 0.0015.
Responses were antagonized by phentolamine (1 μm) but not by (±)‐propranolol (1 μm), haloperidol (10 μm) or α‐flupenthixol (1 μm). This suggested that hyperpolarization was mediated solely throughα‐receptor stimulation not through stimulation of β‐receptors or dopamine‐receptors.
Dose‐ratio shifts produced by phentolamine varied with different agonists. The shift increased in inverse proportion to the ability of the agonists to inhibit [3H]‐(—)‐noradrenaline uptake, suggesting that uptake of agonists limited the dose‐ratio shift. Cocaine and nortriptyline reduced catecholamine‐induced hyperpolarization in concentrations (10 μm and 1 μm respectively) necessary to inhibit [3H]‐(—)‐noradrenaline uptake.
Clonidine (0.01 to 1 μm), oxymetazoline (0.01 to 1 μm) and ergometrine (0.1 to 10 μm) produced a persistent, low‐amplitude hyperpolarization, as though they were partial agonists. Responses to the agonists were blocked by yohimbine (1 μm) but not be prazosin (1 μm).
It is concluded that the adrenergic cell bodies in the ganglion were hyperpolarized through activation of the same type ofα‐receptor (‘α2‐receptors’) as those present at adrenergic nerve terminals.
PROSTAGLANDIN BIOSYNTHESIS BY GUINEA‐PIG SKELETAL MUSCLE in vitro AND THE EFFECT OF OESTRADIOL‐17β AND PROGESTERONE
Authors: KERRY P.J. 
Published: July 2012

The effect of oestradiol and progesterone on prostaglandin biosynthesis by guinea‐pig skeletal muscle in vitro has been investigated.
At high concentrations, oestradiol‐17β (100 μg/ml) and progesterone (500 μg/ml) increased prostaglandin E and prostaglandin F synthesis (measured by radioimmunoassay).
It is suggested that these steroids are unlikely to be found in vivo at levels sufficient to influence prostaglandin synthesis by skeletal muscle in physiological and pathological situations.
[3H]‐QUINUCLIDINYL BENZILATE BINDING TO MUSCARINIC RECEPTORS IN RAT BRAIN: COMPARISON OF RESULTS FROM INTACT BRAIN SLICES AND HOMOGENATES
Authors: GILBERT R.F.T. , HANLEY M.R. , IVERSEN L.L. 
Published: July 2012

The binding of [3H]‐(+)‐quinuclidinyl benzilate ([3H]‐(±)‐QNB) to muscarinic sites in rat brain slice and homogenate preparations was compared.
Evidence is presented in support of the view that only the (—)‐enantiomer of QNB binds with high affinity to muscarinic sites.
The Kd value for [3H]‐(—)‐QNB binding in slices was eight times higher than that measured in homogenates.
Similarly, the potencies of various muscarinic ligands as inhibitors of [3H]‐(—)‐QNB binding were consistently lower in slices than in homogenates.
It is proposed that the results may reflect differences in the binding properties of muscarinic receptors in intact tissue slice and homogenate preparations.
ON THE MECHANISM OF PANCURONIUM‐INDUCED SUPER‐SENSITIVITYTO NORADRENALINE IN RAT SMOOTH MUSCLE
Authors: TOMLINSON D.R. 
Published: July 2012

Pancuronium bromide (5 × 10−5m) caused super‐sensitivityto noradrenaline in the rat isolated vas deferens and hepatic portal vein. This super‐sensitivitywas manifest as a parallel leftward shift of the dose‐response curve for noradrenaline with no alteration of the maximum response to the agonist.
Pancuronium did not potentiate the response of the vas and portal vein to St 91, anα‐adrenocep‐tor agonist which is not a substrate for Uptake x.
Pancuronium did not potentiate the response of the vas to CaCl2.
In vasa deferentia made supersensitive to noradrenaline by treatment with cocaine (1 × 10−5m) pancuronium induced no further potentiation of the response to noradrenaline. However, the super‐sensitivityto noradrenaline induced by pancuronium alone was augmented by the addition of cocaine.
Histofluorescence studies showed that pancuronium inhibited neuronal uptake of α‐methyl noradrenaline in various noradrenergically‐innervated tissues from reserpine‐treated rats.
This study, with support from the literature, suggests that pancuronium induces noradrenaline super‐sensitivityby blockade of Uptake!.
STABILIZATION OF LYSOSOMES IN ANOXIC MYOCARDIUM BY PROPRANOLOL
Authors: WELMAN ELIZABETH 
Published: July 2012

Isolated hearts of guinea‐pigs were perfused aerobically and anoxically for 60 min. (±)‐Propranolol was added to the perfusion medium in concentrations ranging from 10 ng to 10 μg/ml.
Lysosome stability was assessed by measurements of latent acid hydrolase activity in homogenates of left ventricular tissue.
In the absence of propranolol, the integrity of the myocardial lysosomes was considerably reduced after 60 min anoxia. Lysosome stability was enhanced by the presence of (±)‐propranolol. The optimal concentration was found to be 0.1 μg/ml. This concentration of the (+)‐isomer alone was less effective.
It was concluded that bT‐adrenoceptor blockade was the major mechanism by which lysosome disruption was prevented but that some direct membrane effect of propranolol may also be involved.
ACTION OF COLCHICINE AND CYTOCHALASIN B ON THE ACETYLCHOLINE RECEPTOR
Authors: ANWYL ROGER , NARAHASHI TOSHIO 
Published: July 2012

The effects of colchicine and cytochalasin B have been investigated on the extrajunctional acetylcholine (ACh) receptors of rat muscle.Colchicine and cytochalasin B each decreased the amplitude and rise time of the iontophoretic ACh potential. When the dose of ACh was increased in the presence of these agents, ACh potentials were produced with a biphasic waveform consisting of a fast initial phase and a second slow phase.It is proposed that colchicine and cytochalasin B are acting through a mechanism other than the breakdown of microtubules and microfilaments.
POTENTIATION OF RESPONSES TO MONOAMINES BY ANTIDEPRESSANTS AFTER DESTRUCTION OF MONOAMINE AFFERENTS
Authors: JONES R.S.G. , ROBERTS M.H.T. 
Published: July 2012

Stereotaxic lesioning and microiontophoretic techniques were used to study the effects of lesions of the medial forebrain bundle (MFB) on the potentiation by antidepressant drugs of responses to monoamines of cortical neurones.
Active uptake of noradrenaline (NA) and 5 hydroxytryptamine (5‐HT) by synaptosomes from the motor and somatosensory cortex was reduced to approximately 20%, 10 to 14 days following lesion of the MFB in rats.
Unilateral lesions of the MFB caused changes in responsiveness of neurones to NA and 5‐HT, applied by iontophoresis, in the cortex ipsilateral to the lesion. Excitatory responses to both amines were observed less frequently and depression was the predominant response. Excitatory responses on the lesioned side were significantly smaller than on the unlesioned side, but the size of depressant responses was unaltered.
Viloxazine strongly potentiated responses of cortical neurones to NA and 5‐HT on both sides of the brain of MFB‐lesioned rats. There were no significant differences in the potentiation of responses to monoamines on the lesioned or unlesioned sides of the brain.
Desipramine potentiated responses to NA of neurones in the cortex ipsilateral to MFB lesions.
Chlorimipramine potentiated responses to 5‐HT of neurones in the cortex ipsilateral to MFB lesions.
It is concluded that antidepressants can potentiate responses to monoamines despite a profound reduction in presynaptic terminals. The potentiation is unlikely to be the result of blockade of monoamine uptake into presynaptic terminals, and is probably a postsynaptic effect of the antidepressant drugs.
PROSTAGLANDIN E2, PROSTAGLANDIN I2 AND THE VASCULAR CHANGES OF INFLAMMATION
Authors: WILLIAMS T.J. 
Published: July 2012

Plasma exudation and blood flow changes induced by intradermal injection of prostaglandins E2 (PGE2), I2 (PGI2), D2 (PGD2) and F2α (PGF2α) were measured in rabbit dorsal skin by the use of [131I]‐albumin and 133Xe.
Little plasma exudation was produced by any of the prostaglandins when injected alone.
Both PGE2 and PGI2 were potent at increasing blood flow, whereas PGF2α and PGD2 produced an increase only at high doses.
All of the prostaglandins studied potentiated the plasma exudation induced by bradykinin. PGE2 and PGI2 had similar potent potentiating activity, whereas PGD2 and PGF2ae had activity at doses too high to be of biological significance.
Intradermal injections of arachidonate alone resulted in little plasma exudation but produced an increase in blood flow. Arachidonate potentiated bradykinin‐induced plasma exudation.
Locally‐injected indomethacin had no effect on basal blood flow and little effect on the exudation produced by bradykinin, but indomethacin did inhibit the vasodilatation and exudation potentiation produced by arachidonate.
PGE2 and PGI2 had similar potency in producing marked potentiation of plasma exudation induced by intradermal injection of zymosan.
In the reaction to zymosan, it is concluded that vasodilatation is the result of the release of arachidonate, which is subsequently converted to either PGE2 or PGI2. These substances regulate the plasma exudation induced by independently‐released vascular permeability‐increasing mediators.
EFFECTS OF DRUGS ON BEHAVIOUR OF AGGRESSIVE MICE
Authors: KRSIAK M. 
Published: July 2012

The occurrence of 11 aggressive and non‐aggressive activities was observed in aggressive male mice treated with drugs in paired interactions with non‐aggressive males given water. Effects of chlordiazepoxide, diazepam, barbitone, chlorpromazine, imipramine, (‐h)‐amphetamine, lysergic acid diethylamide (LSD) all given orally and of intraperitoneal scopolamine were investigated.
Scopolamine (0.25 and 0.75 mg/kg), (+)‐amphetamine (0.25 and 1 mg/kg), chlorpromazine (2.5 mg/kg), diazepam (10 mg/kg) and chlordiazepoxide (50 mg/kg) reduced aggressive activities (attacks, aggressive unrest) without inhibiting walking across the cage or rearing in the aggressive mice. Thus, the inhibition of aggression induced by these drugs does not seem to be due to neuromuscular impairment and seems to this extent specific. On the other hand, imipramine lessened aggressive activities only at a dose (80 mg/kg) which also decreased walking across the cage and rearing. Barbitone or LSD did not change aggression at either dose tested (20 and 60 or 0.01 and 1 mg/kg, respectively). Aggressive activities were increased significantly only by chlordiazepoxide at a dose of 5 mg/kg.
(+)‐Amphetamine (0.25 mg/kg) and scopolamine (0.75 mg/kg) increased escapes and alert postures, respectively, in the aggressive mice.
Diazepam and chlordiazepoxide decreased tail rattling at 1 and 5 mg/kg, respectively, doses 10 times lower than those inhibiting attacks. The other drugs tested inhibited tail rattling only at doses reducing attacks. Tail rattling appears to be a convenient measure for testing effects of drugs on behavioural conflict.
Diazepam (5 and 10 mg/kg), chlordiazepoxide (20 and 50 mg/kg), barbitone (60 mg/kg) and scopolamine (0.25 and 0.75 mg/kg) increased sociable activities (sniffing, following partners and climbing over them) whereas (+)‐amphetamine, chlorpromazine, imipramine and LSD did not. Effects of the drugs on sociable activities in aggressive mice seem to correlate with their action on punished responding and other types of suppressed behaviour.
PHARMACOLOGY OF 5‐HYDROXYTRYPTAMINE RECEPTORS IN FROG SKIN EPITHELIUM
Authors: DALTON TERENCE 
Published: July 2012

5‐Hydroxytryptamine (5‐HT) stimulates active sodium transport and decreases the passive mucosal to serosal chloride permeability across frog skin. The relative importance of the different regions of the 5‐HT molecule in the mediation of these responses has been studied using a range of structurally related compounds.
Substitution in the ethyl amine side chain of 5‐HT (5‐hydroxytryptophan) results in decreased receptor affinity and intrinsic activity; removal of the side chain (5‐hydroxyindole) abolishes activity. Methoxy substitution of the 5‐OH moiety of 5‐HT has no effect on intrinsic activity but reduces affinity; displacement of the hydroxyl group to position 6 diminishes intrinsic activity and affinity.
It is concluded that both of the 5‐HT‐induced physiological effects are mediated via a single receptor which is distinct from α‐ and β‐adrenoceptors.
THE ROLE OF CELL‐FIXED CALCIUM IN HISTAMINE RELEASE BY COMPOUND 48/80
Authors: GARLAND L.G. , PAYNE A.N. 
Published: July 2012

Histamine release by compound 48/80 was substantially reduced in a time‐dependent manner (maximum at 30 min) by pre‐incubating mast cells in calcium‐free medium at 37°C but not at 2°C. This effect was optimal at pH 7.0 to 7.5.
The re‐introduction of calcium (0.1 to 3 mmol/1) restored histamine release to the control value; this effect was independent of temperature.
Strontium (1 to 30 mmol/1) partially reversed the effect of calcium deprivation but the same concentrations of barium and magnesium depressed histamine release even further. Magnesium (3 to 15 mmol/1) antagonized the effect of calcium replacement.
Results suggest that the level of cell‐fixed calcium involved in compound 48/80‐induced histamine release may be controlled by the combinaton of rapid passive influx and slow active efflux.
STIMULATION OF SPECIFIC [3H]‐OUABAIN BINDING TO MICROSOMAL PREPARATIONS FROM RAT HEART AND SKELETAL MUSCLE BY THYROID HORMONES: EFFECTS OF 6‐HYDROXYDOPAMINE
Authors: BANERJEE SHAILESH P. , SHARMA VIRENDRA K. 
Published: July 2012

Surgical thyroidectomy decreased specific [3H]‐ouabain binding to heart ventricular microsomes by 43% and gastrocnemius muscle microsomes by 34%. Administration of triiodothyronine to euthyroid rats enhanced specific [3H]‐ouabain binding to heart and skeletal muscle membrane by 60% and 33% respectively.
Treatment of thyroidectomized rats with triiodothyronine increased specific [3H]‐ouabain binding by 44% in skeletal muscle membrane preparation and 428% in cardiac microsomes.
Specific [3H]‐ouabain binding decreased by 55% in heart and 53% in gastrocnemius muscle preparations following chemical sympathectomy with 6‐hydroxydopamine.
Treatment with triiodothyronine of euthyroid rats which had been sympathectomized did not significantly alter specific [3H]‐ouabain binding to heart or skeletal muscle membrane preparations.
Administration of triiodothyronine to thyroidectomized and sympathectomized rats increased specific [3H]‐ouabain binding by 80% in heart and 83% in skeletal muscle membrane preparations.
These results suggest that triiodothyronine may influence specific [3H]‐ouabain binding to thyroid hormone nonresponsive tissue such as sympathetic nerve endings. Therefore, the present observations are incompatible with the hypothesis that induction of (Na+ 4‐ K+)‐adenosine triphosphatase of skeletal muscle membrane is the molecular mechanism for the calorigenic actions of thyroid hormones.
EFFECTS OF VERAPAMIL, DANTROLENE AND LANTHANUM ON CATECHOLAMINE RELEASE FROM RAT ADRENAL MEDULLA
Authors: COHEN JACKIE , GUTMAN YEHUDA 
Published: July 2012

The release of catecholamines (CA) from rat adrenal incubated in vitro in Locke solution was studied.
Acetylcholine‐induced release of CA and CA release by 56 mm KC1 were inhibited by verapamil and lanthanum chloride which block calcium permeability.
CA secretion induced by salbutamol or by theophylline was unaffected by either verapamil or lanthanum chloride.
Dantrolene‐sodium inhibited the CA secretion induced by theophylline but only partially reduced potassium‐induced release of CA.
Verapamil enhanced the secretion of CA induced by salbutamol (in a calcium‐free medium).
Tyramine‐induced secretion of CA was unaffected by lanthanum chloride, verapamil or dantrolene‐sodium.
It is suggested that cyclic adenosine 3′,5′‐monophosphate‐mediated CA secretion (induced by theophylline or salbutamol) depends on release of calcium from intracellular stores, and that CA secretion induced by tyramine is independent of intra‐ or extracellular calcium.