bluuebunny/crossref_metadata_2025_split huggingface dataset:
ON THE DISTRIBUTION OF [MET5]‐ AND [LEU5]‐ENKEPHALINS IN THE BRAIN OF THE RAT, GUINEA‐PIG AND CALF
Authors: Di GIULIO A.M. , MAJANE E.M. , YANG H.‐Y.T. 
Published: July 2012

By means of a highly sensitive radioimmunoassay, the content of [met5]‐enkephalin (ME) and [leu5]‐enkephalin (LE) was measured in various regions of the rat, guinea‐pig and calf brain. Provisions were made to differentiate ME from LE by the use of cyanogen bromide (CNBr) to destroy methionine, the carboxy terminal amino acid in the ME sequence. This allows for correction of possible errors due to the cross‐reactivity of the ME to the LE antiserum. Evidence is presented to demonstrate that the specific radioimmunoassay combined with the CNBr technique is a valid method to measure LE and ME content in crude tissue extracts.
In all the species studied, enkephalins appeared to be highly concentrated in the striatum and hypothalamus while very low amounts were found in the cerebellum and hippocampus.
Although the ratio between ME and LE content varied from area to area, the ME content in every region of the rat, guinea‐pig and calf brain was more than 4 fold greater than that of LE.
ACTION OF HISTAMINE RECEPTOR AGONISTS AND ANTAGONISTS ON THE RAT UTERUS
Authors: BERTACCINI G. , MOLINA E. , VITALI T. , ZAPPIA L. 
Published: July 2012

Histamine and a series of compounds acting selectively on Hr and H2‐receptors were tested on the isolated oestrous uterus of the rat.
Histamine had a dose‐dependent inhibitory effect on the contractions elicited by acetylcholine. This action was unaffected by H1‐blockers but was competitively inhibited by H2‐blockers. The H1‐selective agonist, 2‐(2‐aminoethyl)thiazole was ineffective at doses 100 times greater than those of histamine. Conversely, all the H2‐agonists showed activity in the order of potency: N'‐methylhistamine > histamine > N'‐N'‐dimethylhistamine > 5‐methylhistamine > 5‐methyl‐N'‐methylhistamine. Among the non‐imidazole compounds, dimaprit had an activity identical to that of histamine, but all the dimaprit‐like compounds showed negligible activity.
The data obtained suggest that in the rat uterus, (a) the activation of H2‐receptors is responsible for the inhibitory effect of histamine and its analogues; (b) the integrity of the histamine molecule seems to be less crucial than that of the dimaprit molecule for the maintenance of the H2‐activity, since changes in its structure modify but do not abolish the biological activity as they do in the case of dimaprit; (c) the order of activity of the various H2‐receptor agonists is different from that observed in other tissues.
EVIDENCE THAT PROTEASE INHIBITORS REDUCE THE DEGRADATION OF PARATHYROID HORMONE AND CALCITONIN INJECTED SUBCUTANEOUSLY
Authors: PARSONS J.A. , RAFFERTY B. , STEVENSON R.W. , ZANELLI JOAN M. 
Published: July 2012

Agents known to delay absorption from a subcutaneous site were tested in chicks for their ability to prolong the hypercalcaemic response to parathyroid hormone (PTH).
Polyvinylpyrrolidone was found to enhance the response but gelatine greatly reduced the 2 h hypercalcaemia.
The reduction by gelatine was reversed when the protease inhibitor aprotinin was added to the injection vehicle, and hypercalcaemia then persisted for more than 8 h.
Of other protease inhibitors studied, e‐aminocaproic acid was also found to enhance the hypercalcaemic response to subcutaneous PTH and its fragments but, unlike aprotinin, it was ineffective in the presence of gelatine.
By radioimmunoassay and bioassay respectively, it was confirmed that aprotinin raised circulating levels of PTH and also of another peptide hormone, calcitonin, injected subcutaneously.
Addition of calcium to the solutions injected subcutaneously abolished the hypercalcaemic response to PTH while injection of calcium and PTH simultaneously but at separate sites left the response unaltered.
The two protease inhibitors, e‐aminocaproic acid and aprotinin, each restored the response to subcutaneous PTH despite the presence of calcium at the injection site.
It was concluded that protease inhibitors injected subcutaneously with PTH and calcitonin in the chick reduced the rate of degradation of these hormones and that the proteases responsible for hormone degradation at the subcutaneous injection site may be released or activated by calcium ions.
AN ELECTROPHYSIOLOGICAL ANALYSIS OF THE EFFECTS OF MORPHINE ON THE CALCIUM DEPENDENCE OF NEUROMUSCULAR TRANSMISSION IN THE MOUSE VAS DEFERENS
Authors: BENNETT M.R. , LAVIDIS N.A. 
Published: July 2012

The effects of morphine on the Ca‐dependence of the synaptic potential amplitude in the mouse vas deferens have been determined.
The synaptic potential increased with a power factor of 2.4 for [Ca]o between 0.7 mm and 1.8 mm. Morphine (40 nm) decreased the synaptic potential, without altering the second power relationship between the synaptic potential and [Ca]o.
Morphine reversed the depression in the synaptic potential which develops during a short high‐frequency (10 Hz) train of impulses to facilitation. Consequently the synaptic potential beyond the tenth impulse was unaffected by morphine.
Morphine did not alter the facilitation of the synaptic potential which develops during a short low‐frequency (≤2 Hz) train of impulses in normal [Ca]o. Consequently morphine decreased the synaptic potential for each impulse by about the same percentage amount.
Morphine increased the small facilitation in the synaptic potential which occurs during a short low‐frequency (≤2 Hz) train of impulses in high [Ca]o. This facilitation approximated the predictions based on the assumption that each impulse leaves residual Ca ions bound to receptors involved in transmitter release from the nerve terminal.
ADVERSE EFFECTS OF ARTIFICIAL BUFFERS ON CONTRACTILE RESPONSES OF ARTERIAL AND VENOUS SMOOTH MUSCLE
Authors: ALTURA B.M. , ALTURA B.T. , CARELLA A. , TURLAPATY P.D.M.V. 
Published: July 2012

In vitro studies were undertaken on rat aortic strips and portal vein segments in order to determine whether or not several commonly used artificial buffers, i.e., tris(hydroxymethyl) aminomethane (Tris), N‐2‐hydroxyethylpiperazine‐N′‐2‐ethanesulphonic acid (HEPES), morpholine propanesulphonic acid (MOPS), N, N bis(2‐hydroxyethyl) glycine (BICINE) and 1,4‐piperazinediethanesulphonic acid (PIPES), can exert direct actions on vascular smooth muscle.
All artificial buffers used in 5 mm concentrations were found to inhibit development of spontaneous mechanical activity.
Tris, HEPES, MOPS, BICINE and PIPES markedly attenuated contractions induced by adrenaline, angiotensin and KCl. The fast phase components of the agonist‐induced contractions were either obliterated or reduced in the presence of the artificial buffers. The sustained slow phase components were greatly reduced and retarded by the artificial buffers.
The relative order of artificial buffer potency (i.e., from 100% to 14% inhibition) seems to depend upon the agonist and type of smooth muscle.
All of these inhibitory effects were reversible, since normal contractile responses and spontaneous mechanical activity could be obtained by simply reincubating the smooth muscles in Krebs‐Ringer bicarbonate buffer.
A variety of pharmacological antagonists failed to mimic or affect the inhibitory effects of Tris, HEPES, MOPS, PIPES and BICINE.
These data show that five of the most commonly used artificial buffers, to study muscles in vitro, exert adverse effects on contractility of arterial and venous smooth muscle.
3,4‐DIHYDROXYPHENYLACETIC ACID (DOPAC) AND THE RAT MESOLIMBIC DOPAMINERGIC PATHWAY: DRUG EFFECTS AND EVIDENCE FOR SOMATODENDRITIC MECHANISMS
Authors: BEART P.M. , GUNDLACH A.L. 
Published: July 2012

Drug effects on dopamine catabolism of the mesolimbic dopaminergic pathway have been investigated using a sensitive radioenzymatic assay for 3,4‐dihydroxyphenylacetic acid (DOPAC).
Turnover of DOPAC was less rapid in the ventral tegmentum (containing somata and dendrites) than in the nucleus accumbens (containing nerve terminals): 9 and 115 ng g−1 min−1 for ventral tegmentum and nucleus accumbens respectively.
Reserpine (5 mg/kg, 1 h) elevated DOPAC concentration to a greater extent in ventral tegmentum than in nucleus accumbens.
Neuroleptic drugs elevated DOPAC levels in ventral tegmentum and nucleus accumbens. Thioridazine, sulpiride and clozapine, thought to act preferentially on the mesolimbic system, caused a similar elevation in both brain regions.
γ‐Butyrolactone (750 mg/kg) caused a significant decrease in the DOPAC concentration in ventral tegmentum after 0.5 and 1 h, while DOPAC levels in nucleus accumbens were not significantly altered at these time intervals.
Similarities exist between the dopamine catabolism in somatodendritic and nerve terminal regions of mesolimbic dopaminergic neurones in the response to neuroleptic drugs, but differences in catabolism are evident following certain pharmacological treatments such as reserpine and γ‐butyrolactone.
Dopamine release occurs in the somatodendritic region of mesolimbic dopaminergic neurones and release sites may be dendritic as has been found for nigrostriatal dopaminergic neurones.
NICOTINE INHIBITS HYPOXIA‐ AND ARACHIDONATE‐INDUCED RELEASE OF PROSTACYCLIN‐LIKE ACTIVITY IN RABBIT HEARTS
Authors: WENNMALM ÅKE 
Published: July 2012

Rabbit hearts were perfused by the Langendorff technique and the interstitial effluent content of platelet anti‐aggregatory activity (prostacyclin‐like activity) was assayed at regular intervals.
Perfusion was performed with a solution containing 5% C02 in O2. At regular intervals it was changed to a solution containing 12% O2 and 5% CO2 in N2. Alternatively, perfusion with 5% CO2 in O2 was maintained during the entire experiment and sodium arachidonate was infused (5 to 15 μg/min) at intervals. Under the basal conditions no efflux of prostacyclin‐like activity was observed in the interstitial cardiac effluent, but both perfusion with a hypoxic solution and infusion of arachidonate induced such release.
Nicotine (5 × 10−5 m) in the solution perfusing the heart markedly inhibited the efflux of prostacyclin‐like activity into the cardiac interstitial effluent, induced by hypoxia or by infusion of arachidonate.
It is suggested that nicotine counteracts the formation of prostacyclin‐like activity in the rabbit heart by interfering with the enzymatic conversion of arachidonate to prostacyclin.
RELEASE OF PROSTAGLANDIN E FROM THE ISOLATED URINARY BLADDER OF THE GUINEA‐PIG
Authors: ALKONDON M. , GANGULY D.K. 
Published: July 2012

Release of prostaglandin E (PGE) from guinea‐pig urinary bladder in vitro has been demonstrated both in the resting state and during electrical stimulation.
The electrically evoked release of PGE was significantly higher than the resting release and was frequency‐dependent.
The released substance was characterized as PGE pharmacologically by (a) blockade of its response by SC‐19220 on guinea‐pig ileum, (b) reduction of the amount of the released substance by indomethacin and (c) the inhibitory effect of the released substance on adrenergic neurotransmission in guinea‐pig vas deferens.
The prostaglandin seemed to originate from the muscle since tetrodotoxin treatment did not abolish the release during direct muscle stimulation; however, concomitant release from neuronal tissue could not be excluded in the present experiments.
Indomethacin failed to inhibit the mechanical responses of the bladder to transmural stimulation.
The present experiments suggest that PGE is not involved in mediating the non‐cholinergic non‐adrenergic neurotransmission in the guinea‐pig urinary bladder.
A COMPARISON OF CINOBUFOTENINE (THE QUATERNARY DERIVATIVE OF 5‐HT) AND SOME RELATED COMPOUNDS WITH CORYNEINE (THE QUATERNARY DERIVATIVE OF DOPAMINE) ON THE FROG RECTUS, GUINEA‐PIG ILEUM AND RAT FUNDUS STRIP PREPARATIONS
Authors: BARLOW R.B. , BURSTON K.N. 
Published: July 2012

Coryneine is 2.7 times as active as cinobufotenine on the frog rectus but on the guinea‐pig ileum cinobufotenine is 1.5 times as active as coryneine. Cinobufotenine is a potent stimulant of parasympathetic ganglia and its effects are competitively antagonized by hexamethonium.
The effects of pH on activity relative to a standard whose ionisation is constant (Me4N+ or the trimethylammonium analogue of tryptamine) are consistent with the phenate form being weaker than the phenolic form but the changes are smaller than with coryneine because cinobufotenine is a weaker acid.
The hydroxyl group makes a large contribution to activity. Cinobufotenine is 9 times as active as the analogue without a hydroxyl on the frog rectus and 12 times as active as it on the ileum. The 5‐methoxy analogue is an antagonist on the frog rectus and a very weak partial agonist on the ileum.
Cinobufotenine and the quaternary derivative of tryptamine have less than one‐thousandth of the activity of 5‐hydroxytryptamine on the rat fundus strip.
LOCAL KALLIKREIN AND TRYPSIN RESPONSES IN THE RAT
Authors: BENNETT A.J. , WEST G.B. 
Published: July 2012

Locally administered commercial hog pancreatic kallikrein (Depot‐Glumorin) and bovine pancreatic tyrpsin both increased vascular permeability in the skin and paws of rats.
By the use of numerous antagonists and enzyme inhibitors, this vascular response was found to be the result not of kinin formation but of a direct action mostly on histamine receptors.
Highly purified kallikrein did not increase vascular permeability in rats, suggesting either that the effect was due to an impurity in the commercial preparation or that a structural change in the enzyme occurred on purification.
Soya bean trypsin inhibitor prevented the trypsin response when both were injected locally. On intraperitoneal injection, the inhibitor was effective only against local kallikrein.
The kallikrein inhibitor, aprotinin (Trasylol), was not effective against local kallikrein but it reduced the trypsin response when both were injected locally.
STRUCTURE‐ACTIVITY RELATIONSHIPS OF CLONIDINE‐ AND TOLAZOLINE‐LIKE COMPOUNDS AT HISTAMINE AND α‐ADRENOCEPTOR SITES
Authors: MALTA E. , ONG JENNY S.B. , RAPER C. , TAWA PAULINE E. , VAUGHAN G.N. 
Published: July 2012

Thirty clonidine‐ and tolazoline‐like compounds with differing phenyl ring substituents were tested for agonistic actions at histamine H1‐receptors (guinea‐pig ileum), histamine H2‐receptors (guinea‐pig driven right ventricular strips), post‐junctional α‐adrenoceptors (rat desheathed vas deferens) and pre‐junctional α‐adrenoceptors (inhibition of sympathetic stimulation in guinea‐pig driven left atria).
All compounds were inactive at histamine H1‐receptors, while 21 of the 30 compounds displayed varying stimulant activity at H2‐receptors.
At post‐junctional α‐receptors all 30 compounds produced stimulant actions, whereas at prejunctional α‐receptors the compounds displayed either agonistic or antagonistic actions.
Thus structure‐activity relationships (SAR) could only be validated for histamine H2‐ and post‐junctional α‐receptor effects. These studies show that the most potent compounds are those with 2,6‐phenyl substituents in which rotation is restricted so that the two rings are aplanar. Electronic effects of the substituents have a greater influence on activity at H2‐ than at α‐receptors.
The major difference in SAR involves the influence of substituents in the 3, 4 or 5 positions on the phenyl ring. The presence of these substituents abolish significant activity at H2‐receptors, while α‐receptor stimulant activity is retained.
PRESYNAPTIC REGULATION OF THE RELEASE OF ACETYLCHOLINE BY 5‐HYDROXYTRYPTAMINE
Authors: HIRAI K. , KOKETSU K. 
Published: July 2012

The effect of 5‐hydroxytryptamine (5‐HT) on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals and frog sciatic nerve terminals was studied with intracellular microelectrodes.
The change in transmitter release was measured from the mean quantal content calculated by the variance method from evoked fast e.p.s.ps or e.p.ps in low Ca2+‐high Mg2+ Ringer solution.
5‐HT facilitated the release of ACh in low concentrations and depressed it in relatively high concentrations at both preganglionic and motor nerve terminals.
These results suggest the possibility that 5‐HT may play a role in regulating cholinergic transmission in general.
A COMPARISON OF THE SKELETAL NEUROMUSCULAR AND AUTONOMIC GANGLION‐BLOCKING POTENCIES OF FIVE NONDEPOLARIZING RELAXANTS
Authors: BIRMINGHAM A.T. , HUSSAIN S.Z. 
Published: July 2012

Results from in vitro experiments on the phrenic nerve—diaphragm and the hypogastric nerve—vas deferens preparations of the guinea‐pig have been used to plot log concentration‐effect curves for skeletal neuromuscular and ganglion blockade, respectively, for (+)‐tubocurarine, pancuronium, alcuronium, gallamine and fazadinium (AH 8165).
From the log concentration‐effect curves, EC50s and equipotent ratios were calculated. The order of neuromuscular blocking potency was pancuronium = alcuronium > (+)‐tubocurarine > fazadinium = gallamine. The ratio EC50 for ganglion blockade/EC50 for neuromuscular blockade was 2.3 for fazadinium, 6.7 for (+)‐tubocurarine, 22.9 for alcuronium, 24.3 for gallamine and 200.0 for pancuronium.
For pancuronium and gallamine there was a range of concentrations below those producing ganglion blockade at which the response of the vas deferens to hypogastric nerve stimulation was augmented.
The results are compared with some of those available in the literature, measured on other species by other methods.
INTERACTIONS BETWEEN MORPHINE AND THE OPIOID‐LIKE PEPTIDES IN THE RAT VAS DEFERENS
Authors: HUIDOBRO F. , HUIDOBRO‐TORO J. PABLO , MIRANDA H. 
Published: July 2012

Morphine, methadone, levorphanol, pethidine, etonitazene and related morphine‐like alkaloids produced an increase in the electrically‐evoked muscular contraction of the rat vas deferens. In contrast, the enkephalins and β‐endorphin caused inhibition of the twitching.
The concentration of β‐endorphin required to inhibit by 50% the muscular twitch was about 50 to 100 times less than that of the enkephalins.
Pretreatment of the vasa with morphine antagonized the inhibition of the neuromuscular transmission caused by either β‐endorphin or enkephalin.
Conversely, pretreatment with β‐endorphin sensitized the vasa to the increase in twitch tension caused by morphine.
Morphine did not alter the sensitivity to exogenously administered noradrenaline, dopamine or potassium.
EXOCYTOTIC RELEASE OF CATECHOLAMINE FROM PERFUSED ADRENAL GLAND OF GUINEA‐PIG INDUCED BY VERATRIDINE
Authors: ITO S. , NAKAZATO Y. , OHGA A. 
Published: July 2012

Experiments were carried out on perfused adrenal glands of guinea‐pig to determine whether veratridine caused the exocytotic release of catecholamine by comparing its effect with that of splanchnic nerve stimulation and secretagogues such as acetylcholine and excess K+.
Veratridine (100 μm) and excess K+ (56 mm) caused secretion of catecholamine and dopamine‐β‐hydroxylase (DBH) activity in the venous effluents in the presence of atropine (30 μm) and hexamethonium (2 mm). Splanchnic nerve stimulation in the presence or absence of physostigmine (100 nm) and infusion of acetylcholine in the presence of physostigmine had the same effect. In all the responses, the release of DBH tended to last for a longer period than that of catecholamine.
The ratio of catecholamine to DBH activity appearing in the venous effluents was approximately 9, regardless of the method of stimulation. This value was close to the ratio of catecholamines to the ‘soluble’ DBH activity found in the chromaffin granules.
All the types of stimulation used caused a proportional release of adenine nucleotides and catecholamines in the effluents. The adenine nucleotides were mainly adenosine 5′‐phosphate.
The ratio of catecholamine to adenine nucleotides was approximately 11, regardless of the method of stimulation.
It is suggested that the release of catecholamine induced by veratridine occurs by exocytosis in adrenal glands of guinea‐pig.
ELECTRICALLY‐EVOKED RELEASE OF [3H]‐HISTAMINE FROM THE GUINEA‐PIG HYPOTHALAMUS
Authors: BIGGS MARILYN J. , JOHNSON E.S. 
Published: July 2012

[3H]‐histamine was taken up by slices of guinea‐pig hypothalamus against a concentration gradient.
Electrical field stimulation of the superfused slices resulted in an increased efflux of radioactivity, the major part of which was shown to be associated with histamine by paper chromatography.
The evoked release of histamine was dependent on calcium ions in the superfusate and was increased by 56% when the frequency of stimulation was doubled from 5 to 10 Hz.
EFFECTS OF ADRENALECTOMY AND HYPOPHYSECTOMY ON ENKEPHALIN CONTENT OF THE RAT HYPOTHALAMUS
Authors: GIBSON A. , GINSBURG M. , HART S.L. , KITCHEN I. 
Published: July 2012

Hypothalamic content of enkephalin in rats has been measured by bioassay against methionine‐enkephalin on field‐stimulated mouse vas deferens after acid extraction and purification using Amberlite XAD‐2 resin.
Surgical stress lowered hypothalamic enkephalin content initially but 6 days after operation the content was higher in sham‐operated than in adrenalectomized animals.
Corticosteroid replacement therapy showed that hypothalamic enkephalin content was not related directly to circulating corticosteroid levels and that it was increased by the stress of handling and injection.
Hypothalamic enkephalin content of rats that had undergone hypophysectomy 11 days earlier did not differ from that of intact animals but surgical stress, which lowered content in intact rats and had no effect after adrenalectomy, produced a rise in content in these hypophysectomized animals.
The ingestion of 0.9% saline, in place of water, by sham‐adrenalectomized rats altered the effect of surgical stress on hypothalamic enkephalin content without affecting the resting levels.
Of extracts from adrenalectomized rats, 10% contained a substance that behaved atypically on the mouse vas deferens, showing a slower onset and offset of action. The mol. wt. of the substance and sensitivity to naloxone reversal appeared to be similar to enkephalin, but it was resistant to carboxypeptidase‐A and protease treatment.
It is concluded that the enkephalin content of the hypothalamus is affected by activity in the hypothalamus‐pituitary‐adrenal system but that it is not related in a simple manner to the levels of corticotrophin releasing hormone, corticotrophin or corticosteroids.
FAILURE OF ANTI‐INFLAMMATORY STEROIDS TO INHIBIT PROSTAGLANDIN PRODUCTION BY RAT POLYMORPHONUCLEAR LEUCOCYTES
Authors: DRAY F. , McCALL ELAINE , YOULTEN L.J.F. 
Published: July 2012

Like rabbit polymorphonuclear (PMN) leucocytes, rat peritoneal glycogen‐induced PMN leucocytes produced much greater amounts of prostaglandin when incubated with killed bacteria than in the absence of phagocytosable material.
Rat PMN leucocytes produced mainly prostaglandin E2 (PGE2), in amounts up to 17 ng/106 cells in 90 min incubation, some 25 times the amount produced by resting cells.
Indomethacin and meclofenamic acid inhibited prostaglandin production by resting and phagocytosing cells, the IC50 being of the order of 10−6 to 10−7 M for both drugs.
Hydrocortisone and dexamethasone at concentrations up to 10−4 M did not cause significant dose‐related inhibition of prostaglandin production in this system.
It is suggested that the phagocytosing PMN leucocyte is insensitive to the action of anti‐inflammatory steroids with respect to prostaglandin production.