bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE RESPONSES OF THE ISOLATED, BLOOD‐PERFUSED SPLEEN OF THE DOG TO ANGIOTENSIN, OXYTOCIN AND VASOPRESSIN
Authors: DAVIES B.N. , WITHRINGTON P.G. 
Published: July 2012

The responses of the smooth muscle of the capsule and blood vessels of the isolated, blood‐perfused spleen of the dog to angiotensin, oxytocin and vasopressin have been investigated and compared to the actions of the catecholamines, adrenaline and noradrenaline.
Increasing doses of each of the three polypeptides cause graded increases in splenic vascular resistance and reductions in spleen volume.
Doses of the polypeptides which evoked increases in splenic vascular resistance not significantly different from increases produced by chosen doses of each catecholamine caused significantly smaller reductions in spleen volume.
The time‐course of action of the polypeptides on the splenic vascular smooth muscle is different since the time to 50% recovery from vasopressin is highly significantly longer than that for equieffective doses of either angiotensin or oxytocin.
Phenoxybenzamine, in a dose which almost blocked the actions of the catecholamines, increased the responses of the vascular and capsular smooth muscle to oxytocin, vasopressin and angiotensin. This increase was not observed with another α‐adrenoceptor blocking agent, phentolamine.
The significant species variation in the responses of the smooth muscle of the spleen to polypeptides and catecholamines are discussed and the results are considered in the context of the possible physiological roles of the polypeptides in haemorrhage.
EVIDENCE FOR NORADRENALINE AND ADRENALINE AS SYMPATHETIC TRANSMITTERS IN THE CHICKEN
Authors: DeSANTIS V.P. , LÄNGSFELD W. , LINDMAR R. , LÖFFELHOLZ K. 
Published: July 2012

The concentrations of noradrenaline and adrenaline in various organs, arterial plasma and venous outflow from isolated hearts of adult chickens have been determined.
The relative adrenaline concentrations (percentage of the sum of noradrenaline and adrenaline) in the heart (33%), spleen (16%) and brain (26%) were higher than those found in mammalian organs. Chemical sympathectomy by pretreatment with 6‐hydroxydopamine caused a decrease of the noradrenaline and adrenaline concentrations in the heart to 20 and 23% and in the spleen to 16 and 29%, respectively.
Stimulation of the right sympathetic nerves, infusion of tyramine or infusion of a modified Tyrode solution containing 108 mM K+ and 44 mM Na+ caused an output of both noradrenaline and adrenaline into the perfusate of isolated hearts. The relative adrenaline concentration in the perfusate (20–28%) was not significantly different from the relative adrenaline concentration remaining in these hearts (19–22%). In the individual experiments, the noradrenaline: adrenaline ratios of the stimulation perfusates were positively correlated with the ratios found in the hearts.
The effects of noradrenaline and adrenaline on cardiac rate and tension development were studied in spontaneously beating right atria and electrically driven left atria, respectively. In addition, the arterial pressure rise in response to noradrenaline or adrenaline was measured in chickens. It was found that the cardio‐vascular potency of noradrenaline, as reflected by the increases in heart rate, cardiac tension development and arterial blood pressure, was not significantly different from that of adrenaline.
It is concluded that, in the chicken heart and spleen, both noradrenaline and adrenaline act as sympathetic neurotransmitters.
BEHAVIOURAL CHANGES INDUCED IN CONSCIOUS MICE BY INTRACEREBROVENTRICULAR INJECTION OF CATECHOLAMINES, ACETYLCHOLINE AND 5‐HYDROXYTRYPTAMINE
Authors: HERMAN Z.S. 
Published: July 2012

A simple method of injecting soluble substances into the lateral ventricle of the brain of the conscious mouse is described.
The effect of various doses of noradrenaline, dopamine, acetylcholine, 5‐hydroxytryptamine given into the right lateral brain ventricle were tested on locomotor and exploratory activities of mice.
Noradrenaline in a dose of 0.1 μg increased locomotor activity. This effect was prevented by phenoxybenzamine but not by propranolol.
Higher doses of noradrenaline (1 or 10 μg) decreased locomotor and exploratory activities. Propranolol but not phenoxybenzamine abolished these effects.
Dopamine (0.1 or 1 μg) increased locomotor activity. The higher doses also induced tremor.
The highest dose of dopamine tested (10 μg) elicited stereotypical behaviour.
All the behavioural phenomena induced by 0.1 μg and 10 μg of dopamine were blocked by pimozide.
Acetylcholine (1 and 10 μg) and 5‐hydroxytryptamine (1 μg) inhibited locomotor and exploratory activity.
The effects of 1 and 10 μg of acetylcholine were abolished by atropine (5 mg/kg i.p.). Methysergide (5 mg/kg i.p.) had no influence on the effects of 5‐hydroxytryptamine (1 μg).
INHIBITION BY APOMORPHINE OF THE METOCLOPRAMIDE‐INDUCED CATALEPSY AND INCREASE IN STRIATAL HOMOVANILLIC ACID CONTENT
Authors: AHTEE LIISA 
Published: July 2012

The mechanism of the cataleptic effect of metoclopramide was analyzed by using drugs which alter the activity of dopaminergic or cholinergic neurones or the content of γ‐aminobutyric acid in the central nervous system of rats.
The cataleptic effect of metoclopramide (20 mg/kg) was antagonized by apomorphine (10 mg/kg) and by atropine (50 mg/kg). Aminooxyacetic acid (AOAA, 25–50 mg/kg) potentiated the catalepsy induced by metoclopramide (5 mg/kg).
Metoclopramide alone did not alter the rectal temperature of rats. It did not alter the AOAA‐induced hypothermia, but it partially antagonized apomorphine‐induced hypothermia.
Metoclopramide induced a six‐fold increase in striatal homovanillic acid (HVA) concentration, but it did not change the dopamine or noradrenaline content in the brain of rats. Apomorphine decreased the striatal HVA concentration in control and in metoclopramide‐treated rats. Atropine and AOAA did not alter the metoclopramide‐induced increase in striatal HVA concentration.
The results suggest that metoclopramide produces catalepsy by blocking striatal dopamine receptors.
TOLERANCE TO MORPHINE‐INDUCED CALCIUM DEPLETION IN REGIONAL BRAIN AREAS: CHARACTERIZATION WITH RESERPINE AND PROTEIN SYNTHESIS INHIBITORS
Authors: ROSS D.H. 
Published: July 2012

Administration of a single dose of morphine sulphate (25 mg/kg) induces tolerance to calcium depletion lasting seven days.
There are no apparent changes in calcium content in any of eight discrete brain regions throughout this seven day period.
Pretreatment with reserpine (5 mg/kg) did not alter the ability of morphine to induce tolerance. Reserpine alone produced no tolerance to its own calcium depleting action.
Cycloheximide (500 μg/kg) but not chloramphenicol (200 mg/kg) effectively prevented development of tolerance.
It is concluded that the induction of tolerance to calcium depletion seen after morphine may involve changes in various proteins in membranes of synaptic origin.
AN INVESTIGATION OF THE TACHYCARDIA PRODUCED BY INTRACEREBRO‐VENTRICULAR INJECTIONS OF ISOPRENALINE IN MICE
Authors: BURDEN D.T. , PARKES M.W. 
Published: July 2012

Isoprenaline, 3.5–20 ng, injected intracerebroventricularly in atropinized mice under pentobarbitone anaesthesia produced a dose‐dependent tachycardia.
Pretreatment with either reserpine or pempidine blocked nervously‐mediated tachycardia as shown by marked reduction of that due to stimulation of the spinal outflow in pithed mice. After pretreatment with these drugs, intracerebroventricular isoprenaline caused tachycardia of a similar degree and time course to that in mice not so pretreated.
Pretreatment with either reserpine or pempidine caused supersensitivity to the tachycardia due to intravenous isoprenaline.
When allowance was made for this supersensitivity in the effect of intracerebroventricular isoprenaline in pretreated mice, a small dose‐dependent residual effect remained that could be attributed to leakage of isoprenaline into the peripheral circulation.
This was confirmed by the appearance of a late‐developing tachycardia on intracerebroventricular injection of isoprenaline in spinal mice.
It is therefore concluded that the tachycardia caused by intracerebroventricular isoprenaline in mice is, at least initially, of central origin.
EFFECTS OF RESERPINE ON THE ADRENAL MEDULLA OF THE SPONTANEOUSLY HYPERTENSIVE RAT
Authors: SLOTKIN T.A. 
Published: July 2012

Reserpine administration resulted in a larger initial decline in adrenal catecholamines in spontaneously hypertensive rats (SHR) than in normotensive Wistar rats (NWR); the difference was eliminated by pretreatment with chlorisondamine.
Reserpine also produced a larger increase in SHR catecholamines and dopamine β‐hydroxylase several days later; chlorisondamine pretreatment did not prevent the increases, although it did slightly slow the increases.
Vesicles from SHR or NWR incubated with reserpine in vitro demonstrated equivalent inhibition of adenosine 5′‐triphosphate (ATP)‐Mg2+ ‐stimulated adrenaline uptake.
Recovery of uptake was more rapid in SHR than in NWR after reserpine inhibition, and this was associated with a burst of new vesicle synthesis in the SHR; chlorisondamine pretreatment reduced the number of new, immature vesicles in reserpine‐treated SHR.
Both SHR and NWR secreted equal proportions of their adrenal catecholamine contents after nicotine administration.
These data suggest that the sympatho‐adrenal system of the SHR exhibits an enhanced reflex response to reserpine but that reserpine is equally effective in SHR and NWR in producing blockade of vesicular catecholamine transport; these alterations can affect markedly the actions of autonomic drugs in the SHR.
NICOTINE‐INDUCED STIMULATION OF STEROIDOGENESIS IN ADRENOCORTICAL CELLS OF THE CAT
Authors: RUBIN R.P. , WARNER W. 
Published: July 2012

The effect of nicotine on steroid production and release from trypsin‐dispersed cat adrenocortical cells was investigated.
Nicotine, like adrenocorticotrophin (ACTH), elicited a dose‐dependent increase in steroidogenesis, which depended upon the presence of calcium in the medium.
Augmented steroid production evoked by submaximal concentrations of ACTH, monobutyryl cyclic adenosine 3′,5′‐monophosphate (AMP), or prostaglandin E2 was further enhanced by steroidogenic concentrations of nicotine.
These results are discussed in relation to the possible mode of action of nicotine on cortical cells and to the potential consequences of smoking during stress.
ACTION OF β‐ADRENOCEPTOR ANTAGONISTS ON THE RESPONSE TO ISOPRENALINE IN THE OESTROGEN DOMINATED RABBIT UTERUS
Authors: NESHEIM BRITT—INGJERD 
Published: July 2012

Log dose‐response curves to isoprenaline from spontaneously contracting muscle strips from rabbit uterus have been obtained. The effects of the α‐adrenoceptor antagonists phentolamine and phenoxybenzamine, the β‐adrenoceptor antagonists propranolol and practolol, and (+)‐propranolol on the log dose‐response curves were studied.
Phentolamine 5.3 × 10−7 M had a stimulating effect on the muscle strips, moving the log dose‐response curve of isoprenaline to the right. Phenoxybenzamine 2.9 × 10−5 M had no effect on the curves.
Propranolol 3.4 × 10−6 M had no effect on the curves from circular muscle strips, with either phentolamine 5.3 × 10−7 M or with phenoxybenzamine 2.9 × 10−5 M as α‐blocker. The curves from the longitudinal muscle strips were shifted somewhat to the right, the same shift, however, being obtained with (+)‐propranolol 3.4 × 10−6 M.
Practolol 3.8 × 10−6, 3.8 × 10−5 and 3.8 × 10−4 M was without effect on the curves, either in the circular or in the longitudinal strips.
It is concluded that neither propranolol at 3.4 × 10−6 M nor practolol act as β‐adrenoceptor antagonists in oestrogen dominated rabbit uterus. In all other tissues investigated, propranolol or practolol block the effect of isoprenaline. Whether the effect of isoprenaline in this tissue may be termed a β‐effect, is then a question of definition. In addition there is no evidence for any extraneuronal uptake mechanisms for isoprenaline.
Variations in sensitivity to β‐stimulation with the time of the year were observed, the sensitivity being greatest in the winter and lowest in the summer.
THE EFFECT OF PROPRANOLOL ON VASCULAR RESPONSES TO SYMPATHETIC NERVE STIMULATION
Authors: DAWES P.M. , FAULKNER D.C. 
Published: July 2012

In an attempt to clarify the rǒle of the sympathetic neurone in the antihypertensive action of propranolol, the effect of this drug on responses to lumbar sympathetic nerve stimulation has been studied in the perfused hind‐limb of the dog.
No consistent reduction of maximal or submaximal responses to nerve stimulation was produced by propranolol (10 to 100 μg/kg). In contrast, potentiation of nerve‐evoked responses, as well as those to injected noradrenaline, usually occurred. Dexpropranolol (50 μg/kg) had no effect.
When neuronal uptake of noradrenaline was inhibited by desmethylimipramine or cocaine, no reduction in responses to sympathetic nerve stimulation was observed with propranolol.
No evidence was found, using α‐adrenoceptor blocking drugs, that released transmitter stimulates β‐adrenoceptors in the blood vessels of the hind‐limb.
No evidence has been found for the existence of an adrenergic neurone‐blocking action of propranolol that might contribute to the antihypertensive activity in man.
ENHANCED INACTIVATION OF PROSTAGLANDIN E2 BY THE RABBIT LUNG DURING PREGNANCY OR PROGESTERONE TREATMENT
Authors: BEDWANI J.R. , MARLEY P.B. 
Published: July 2012

The inactivation of prostaglandin E2 by the rabbit lung was estimated in vivo by comparing its depressor potency following intravenous and intra‐aortic injections, and in vitro by measuring the rate of disappearance of smooth muscle stimulating activity when the prostaglandin was incubated with high speed supernatant fractions from lung homogenates.
The ability of the lung to inactivate prostaglandin E2 in vivo increased gradually throughout pregnancy, and then decreased rapidly during the three days post‐partum.
An increased lung inactivation was also seen in pseudopregnant (day 12) rabbits, and in non‐pregnant rabbits treated with progesterone for 12 days. A further increase occurred when progesterone treatment was prolonged to 26 days.
Treatment with oestradiol monobenzoate or cortisol for 12 days, and deprivation of ovarian hormones for 14‐17 days by ovariectomy, were without effect on the lung inactivation of prostaglandin E2.
The in vitro experiments revealed a striking increase in the activity of lung prostaglandin metabolizing enzymes during pregnancy.
The results are discussed in relation to the hormonal changes occurring during pregnancy, and it is suggested that an enhanced lung inactivation of prostaglandins might have an important protective function at this time.
INDOMETHACIN‐INDUCED INCREASE IN NORADRENALINE TURNOVER IN SOME RAT ORGANS
Authors: FREDHOLM B.B. , HEDQVIST P. 
Published: July 2012

The effect of a prostaglandin synthesis inhibitor, indomethacin, on noradrenaline turnover rate in various rat tissues was determined from the product of the endogenous noradrenaline concentration and of the rate constant of (—)‐[3H]‐noradrenaline decline after injection of the labelled amine in tracer doses.
Treatment of the rats with indomethacin (5 mg/kg p.o. five times during 2.5 days) increased noradrenaline turnover rate 32–36% in submandibular gland, spleen and heart, and 4–17% in epididymal and subcutaneous adipose tissue.
The extrapolated [3H]‐noradrenaline content at time 0 was greater in heart and adipose tissue of indomethacin‐treated animals than in controls, while it was not significantly changed in spleen and salivary gland.
There was no apparent relationship between tissue concentrations of intravenously injected [14C]‐indomethacin and the effect of indomethacin on noradrenaline uptake and turnover rate in the different tissues.
Indomethacin treatment did not affect monoamine oxidase and catechol O‐methyl‐transferase activities in the different tissues.
The results are consistent with the hypothesis that indomethacin increases noradrenaline turnover in the rat by blockade of a locally operating feed back inhibition of transmitter release by prostaglandins. However, additional effects, such as an increased impulse traffic, cannot be ruled out.
INHIBITION OF THE PULMONARY INACTIVATION OF PROSTAGLANDINS in vivo BY DI‐4‐PHLORETIN PHOSPHATE
Authors: CRUTCHLEY D.J. , PIPER PRISCILLA J. 
Published: July 2012

Inactivation of prostaglandin E2 in the pulmonary circulation of rabbits in vivo was measured by comparing the hypotensive effects of doses given intravenously and intra‐arterially.
Di‐4‐phloretin phosphate (DPP) 25–100 μg kg−1 min−1 inhibited the inactivation of prostaglandin E2 in the pulmonary circulation.
These doses of DPP caused a marked shift to the left of the dose‐response curve to prostaglandin E2 given intravenously but did not affect the dose‐response curve to prostaglandin E2 given intra‐arterially.
Inhibition of pulmonary inactivation of prostaglandins E2 and E2α caused marked potentiation of their gastrointestinal effects.
At these doses antagonism of the hypotensive action of prostaglandin E2 by DPP was seldom seen but the gastrointestinal effect of prostaglandin E2α was sometimes antagonized.
After treatment with DPP 100 μg kg−1 min−1, high doses of prostaglandin were sometimes lethal.
AN ANALYSIS OF THE DEPRESSOR RESPONSES TO HISTAMINE IN THE CAT AND DOG: INVOLVEMENT OF BOTH H1‐ AND H2‐RECEPTORS
Authors: BLACK J.W. , OWEN D.A.A. , PARSONS M.E. 
Published: July 2012

The depressor responses to histamine, in anaesthetized cats and dogs, have been shown to involve both histamine H1‐ and H2‐ receptors.
In both species, histamine caused dose‐dependent falls in blood pressure. The dose‐response curve could be displaced to the right by administration of mepyramine 2.5 × 10−6 mol/kg i.v. The displacement was maximal with a dose‐ratio of less than ten.
Metiamide alone, up to 2 × 10−6 mol kg−1 min−1, had no significant effect on the histamine dose‐response curve.
When administered in the presence of mepyramine, metiamide, 4 × 10−7 and 2 × 10−6 mol kg−1 min−1, caused dose‐dependent displacements to the right, of the histamine dose‐response curve greater than could be achieved with mepyramine alone.
The results indicate the presence of both histamine H1‐ and H2‐receptors in the cardiovascular system of the cat and dog. Both receptors produce a common response, i.e. a fall in blood pressure.
PRESSOR RESPONSE INDUCED BY LOCAL ANAESTHETICS PERFUSED THROUGH THE CEREBRAL VENTRICLES OF DOGS
Authors: HARANATH P.S.R.K. , INDIRA‐NARAYAN G. , VENKATAKRISHNA‐BHATT H. 
Published: July 2012

The antihistamines mepyramine and halopyramine which have local anaesthetic properties, produced a rise in arterial blood pressure followed by a fall, similar to that seen with procaine, when perfused in a 10 mg/ml solution from the lateral ventricle to the cisterna magna in dogs.
The pressor response produced by procaine perfused through the cerebral ventricle is due to an action on structures situated in the caudal half of the floor of the fourth ventricle because a pressor response was obtained when a few microlitres of a 50 mg/ml solution of procaine were applied to a small area of the exposed floor of the fourth ventricle in a region 2 to 4 mm rostral to obex, and after cauterization of this area procaine perfused through the cerebral ventricles no longer raised arterial blood pressure.
Bilateral denervation of the carotid sinus did not affect the pressor response obtained with procaine perfused through the cerebral ventricles.
The pressor response to procaine is mediated through the sympathetic nervous system. It results partly from an increased adrenaline discharge from the adrenal glands and partly from increased sympathetic vasomotor tone, because the response is abolished or attenuated after removal of the adrenal glands and intravenous injections of hexamethonium and phentolamine.
THE ACTION OF 5‐HYDROXYTRYPTAMINE ON CHEMORECEPTOR DISCHARGES OF THE CATS CAROTID BODY
Authors: NISHI K. 
Published: July 2012

Chemoreceptor discharges were recorded in vivo from fine filaments of the carotid sinus nerve containing a single or several active units; their frequency was used as an index of receptor activity. The effects of 5‐hydroxytryptamine (5‐HT) on chemoreceptors were studied in 26 adult cats. At times, sinus baroreceptor discharges were recorded from the carotid nerve and the effect of 5‐HT on the discharges was examined.
Intra‐carotid injections of 5‐HT (2–20 μg) induced a sharp and brief increase in chemoreceptor discharges, followed by depression or block which lasted for several seconds. Repeated injections at short intervals, and a small dose after a large dose of 5‐HT resulted in depressed or blocked response to 5‐HT.
5‐HT in high doses (10–20 μg, La.) slightly depressed the chemoreceptor discharges induced by either acetylcholine (ACh) or NaCN, when these substances were applied within 20 s after 5‐HT. 5‐HT (5–20 μg, i.a.) applied during asphyxia induced a further increase in chemoreceptor discharges, soon followed by block of the discharges lasting for several seconds.
Atropine or hexamethonium in high doses did not change the chemoreceptor response to 5‐HT, while that to ACh was markedly depressed.
(+)‐Lysergic diethylamide (LSD), methysergide or gramine did not alter the response to 5‐HT, while LSD in low doses produced a marked increase in chemoreceptor discharges.
Acute and chronic treatment with reserpine (5–10 mg/kg, i.v.) of the animals did not change the sensitivity and the reactivity of the chemoreceptor to ACh and NaCN, while the chemoreceptor response to 5‐HT was augmented, indicating an increase in the sensitivity of chemoreceptors to 5‐HT.
5‐HT in small doses (2–10 μg, i.a.) induced a marked increase in sinus baroreceptor discharges; subsequently discharges were depressed or blocked for several seconds.
The results are discussed in relation to possible mechanism of action of 5‐HT on the chemoreceptors. It is concluded that the exogenous 5‐HT probably acts directly on the chemosensory nerve endings and depolarizes them, but 5‐HT contained in the carotid body does not play a significant role in the generation of chemoreceptor discharges.
REDUCTION IN THE CHOLINESTERASE ACTIVITY OF THE RAT ANOCOCCYGEUS MUSCLE PRODUCED BY CORTICOSTERONE
Authors: GIBSON A. , POLLOCK D. 
Published: July 2012

Administration of corticosterone caused a 47% reduction in the cholinesterase (ChE) activity of homogenates of the rat anococcygeus muscle.
ChE activity was also reduced by morphine withdrawal and this effect was abolished by the corticosteroid synthesis inhibitor, metyrapone.
A single dose of reserpine reduced ChE activity in normal but not in adrenalectomized rats.
ChE activity was increased by adrenalectomy or by metyrapone treatment.
The mechanism of the corticosteroid‐induced reduction in ChE activity is discussed.
The reduction in ChE activity produced by corticosterone, morphine withdrawal, or a single dose of reserpine might explain the leftward shift of the dose‐% response curve to acetylcholine produced by these procedures in the isolated anococcygeus muscle of the rat.