bluuebunny/crossref_metadata_2025_split huggingface dataset:
DEVELOPMENT OF NICOTINIC RESPONSES IN THE RAT ADRENAL MEDULLA AND LONG‐TERM EFFECTS OF NEONATAL NICOTINE ADMINISTRATION
Authors: ROSENTHAL R.N. , SLOTKIN T.A. 
Published: July 2012

The development of nicotinic responses in the rat adrenal medulla was examined at various ages from 1 to 50 days of age by testing the ability of nicotine (10 mg/kg, s.c.) to deplete catecholamines and induce tyrosine hydroxylase.
Catecholamines were depleted 25% 3 h after injection of nicotine at all ages tested, but the degree of tyrosine hydroxylase induction 24 h after nicotine increased with age.
These data indicate that functional nicotinic receptors are present in the neonatal adrenal medulla before the development of functional splanchnic innervation, but that the development of the ability to induce tyrosine hydroxylase is not coupled directly to the development of secretory mechanisms.
The long‐term effects of a single dose of nicotine (10 mg/kg, s.c.) administered to one day old rats were also examined.
After the short‐term catecholamine depletion caused by nicotine, there were persistent elevations of catecholamines and tyrosine hydroxylase until 23 days of age; however, dopamine β‐hydroxylase remained elevated into young adulthood.
These data indicate that neonatal nicotine administration can produce long‐term changes in adrenal catecholamine biosynthetic enzymes.
A COMPARISON OF THE EFFECTS OF BRADYKININ, 5‐HYDROXYTRYPTAMINE AND HISTAMINE ON THE HEPATIC ARTERIAL AND PORTAL VENOUS VASCULAR BEDS OF THE DOG: HISTAMINE H1 AND H2‐RECEPTOR POPULATIONS
Authors: RICHARDSON P.D.I. , WITHRINGTON P.G. 
Published: July 2012

The hepatic arterial and hepatic portal venous vascular beds of anaesthetized dogs were separately perfused in different experiments.
From measurements of perfusion pressures and blood flows in the two series of experiments, hepatic arterial vascular resistance (HAVR) and hepatic portal venous vascular resistance (HPVR) respectively were calculated.
Bradykinin, 5‐hydroxytryptamine (5‐HT) and histamine were injected intra‐arterially and intraportally and dose‐response curves constructed from these data.
Bradykinin injected intra‐arterially caused dose‐dependent hepatic arterial vasodilatation, and with an ED50 of 2.66 × 10−13 mol was more potent than any other vasodilator agent yet examined on this vascular bed.
Bradykinin injected intraportally at doses up to 10 times those which were maximal on the arterial circuit did not alter the calculated HPVR.
5‐HT injected intra‐arterially caused weak and variable rises in HAVR, indicating vasoconstriction. The maximum rise in HAVR was much less than that attained with noradrenaline in the same preparations.
5‐HT injected intraportally caused dose‐dependent rises in HPVR indicating portal constriction at doses above 15–100 μg: in some experiments small doses of 5‐HT resulted in reductions in calculated HPVR.
Histamine has previously been shown to cause hepatic arterial vasodilatation: by intraportal injection, it caused dose‐dependent rises in HPVR.
In order to examine the receptors responsible for the effects of histamine, dose‐response curves were constructed before and after mepyramine and metiamide.
On the hepatic arterial vascular bed, metiamide did not antagonize the vasodilator effects of intra‐arterial histamine, but these effects were antagonized by mepyramine.
Similarly on the hepatic portal bed, the rises in HPVR due to histamine were antagonized by mepyramine but not by metiamide.
The effects of histamine on both the hepatic arterial and portal venous vascular beds of the dog are therefore mediated predominantly by histamine H1‐receptors.
[3H]‐OUABAIN BINDING TO PERIPHERAL ORGANS OF CATS: EFFECT OF ETHANOL
Authors: BANERJEE SHAILESH P. , SHARMA VIRENDRA K. 
Published: July 2012

The specific [3H]‐ouabain binding to microsomal fractions derived from cat heart, liver, spleen, and kidney increased significantly following chronic administration of ethanol.
Since ouabain binds exclusively to cell membrane (Na+ + K+)‐adenosine triphosphatase ((Na+ + K+)‐ATPase), these results provide evidence for an increase in number of (Na+ + K +)‐ATPase macromolecules during chronic alcoholism.
The importance of the increase in number of (Na+ + K+)‐ATPase molecules in the adaptive increase in ethanol metabolism and cardiac myopathy in chronic alcoholism is discussed.
EFFECTS OF OXYPERTINE ON THE ISOLATED VAS DEFERENS OF THE RAT
Authors: MIRANDA H. 
Published: July 2012

The isolated vas deferens of the rat was used to examine the peripheral action of oxypertine, a psychotropic‐anxiolytic drug.
Oxypertine (4.4 × 10−10m to 2.6 × 10−5m) antagonized competitively the effects of noradrenaline (pA2 = 7.2), 5‐hydroxytryptamine (pA2 = 8.6) and dopamine (pA2 = 9.8).
Oxypertine (8.8 × 10 −9m to 2.6 × 10−5m) antagonized the effects of low concentrations of acetylcholine and enhanced the contractions elicited by high concentrations of acetylcholine.
The contractions evoked by transmural stimulation of the vas deferens were reduced by oxypertine.
Oxypertine failed to antagonize the responses to potassium chloride.
These findings are compared with the effects of other antidepressant drugs.
HEPATIC DRUG METABOLISM AND HAEM BIOSYNTHESIS IN LEAD‐POISONED RATS
Authors: GOLDBERG A. , MEREDITH P.A. , MILLER S. , MOORE M.R. , THOMPSON G.G. 
Published: July 2012

Pretreatment of rats with intraperitoneal injections of lead was shown to result in a depression of the microsomal mixed function oxidase system, as assessed by a decrease in hepatic microsomal P‐450 and b5 content and by a decrease in the activity of the enzymes aniline hydroxylase and aminopyrine demethylase. Lead had a more marked effect on cytochrome P‐450 than b5.
The activity of the rate‐limiting enzyme of haem biosynthesis, δ‐aminolaevulinic acid synthase, was inversely correlated with the microsomal cytochrome P‐450 content.
The activity of the haem biosynthetic enzymes δ‐aminolaevulinic acid dehydratase, coproporphyrinogen oxidase and ferrochelatase were decreased by increasing lead pretreatment.
The activity of the haem catabolic enzyme, haem oxygenase, was increased by lead pretreatment.
BLOCKADE OF DESENSITIZATION OF NICOTINIC RECEPTORS OF THE CAT ADRENAL MEDULLA BY CONCANAVALIN A
Authors: KIRPEKAR S.M. , PRAT J.C. 
Published: July 2012

The possibility of concanavalin A (Con A) blocking the development of desensitization of nicotinic receptors of the cat adrenal gland has been investigated.
During perfusion of the adrenal gland with Krebs‐bicarbonate solution containing acetylcholine (ACh), the rate of catecholamine (CA) secretion was very high in the first 2 min; thereafter, as perfusion with ACh was continued the output fell, to reach about 20% of the initial value in 10 minutes. When the adrenal gland was pretreated with Con A, the subsequent desensitization of release during continued infusion of ACh was prevented.
When the adrenal gland was perfused with high K+ solution, there was always a large initial secretion of CA, and as perfusion with high K+ continued the output fell, to reach about 15% of the initial rate in 10 minutes. Con A did not affect the rate of CA secretion induced by high K+.
It is tentatively suggested that Con A blocks the desensitization of CA secretion evoked by ACh by interaction with the glycoprotein moiety of the nicotinic receptor of adrenal chromaffin cells.
TIME COURSE OF DEGENERATION OF SHORT AND LONG POSTGANGLIONIC SYMPATHETIC NERVE FIBRES AND EFFECT OF PENTOBARBITONE AND COLCHICINE ON DEGENERATION
Authors: WAKADE ARUN R. 
Published: July 2012

The time‐course of degeneration of sympathetic nerves was investigated by measurement of the endogenous noradrenaline content of the rat vas deferens, submandibular gland and spleen following sympathectomy.
Extirpation of the hypogastric plexus, superior cervical ganglion and coeliac plexus under pentobarbitone anaesthesia caused 50% depletion of the noradrenaline content of the vas deferens, submandibular gland and spleen in approximately 16, 19 and 21 h, respectively.
Under pentobarbitone anaesthesia, proximal sympathectomy (i.e., close to the end organ) produced depletion of the noradrenaline content of the submandibular gland 8 h earlier than that caused by distal sympathectomy. Under ether anaesthesia, the time difference in obtaining the same degree of depletion after the two procedures of sympathectomy was only 2 hours.
Removal of the superior cervical ganglion under ether anaesthesia resulted in almost complete depletion of noradrenaline content of the submandibular gland in 17 h, whereas when a similar operation was performed under pentobarbitone anaesthesia, nearly 24 h were required for the same degree of depletion. Similarly, the noradrenaline content of the spleen was depleted 4 h earlier if the coeliac plexus was ablated under ether as compared to pentobarbitone anaesthesia.
Local application of colchicine (10 mg/ml, 30 min) to postganglionic sympathetic nerve axons had no effect on the noradrenaline content of the submandibular gland up to 24 hours. However, removal of the superior ganglion following colchicine application considerably slowed the depletion of the noradrenaline content of the submandibular gland (at 17 and 20 h after ganglionectomy, 10 and 20% depletion, respectively, in the experimental gland, as compared to 70 and 80%, respectively, in the control gland).
To explain the results, it is proposed that injury to the sympathetic nerves at the site of sectioning triggers a signal (messenger substance) which travels down to the nerve endings to produce degeneration. Thus, the length of the extrinsic nerve fibre influences the time course of degeneration by changing the rate of transport of the messenger substance, whereas pentobarbitone and colchicine alter the synthesis and/or transport of the messenger substance to modify the time‐course of degeneration.
EFFECTS OF MAGNESIUM ON CONTRACTILE RESPONSES INDUCED BY ELECTRICAL TRANSMURAL STIMULATION AND NORADRENALINE IN RABBIT THORACIC AORTA
Authors: FUJIWARA MOTOHATSU , KITAGAWA HISATO , KURAHASHI KAZUYOSHI 
Published: July 2012

In rabbit isolated thoracic aortae, effects of magnesium ions on the contraction and 3H‐efflux in response to electrical transmural stimulation and on the contractile responses induced by noradrenaline and KCl were investigated.
Addition of magnesium (1.2, 3.6, 12.0 and 24.0 mm) to the bathing solution inhibited the electrically induced contractions in a dose‐related manner; the inhibition was complete with a concentration of 24.0 mm.
The increase in 3H‐efflux induced by electrical transmural stimulation was inhibited by the addition of magnesium to the superfusing fluid, but a complete block was not obtained even in high concentrations of magnesium.
Magnesium ions (1.2, 3.6, 12.0 and 24.0 mm) inhibited the contractile responses induced by low concentrations of noradrenaline (2 × 108m) and KCl (2 × 10 −2m). However, the responses induced by higher concentrations of noradrenaline (5 × 10−7 and 10−5m) and KCl (3 and 4 × 10−2m) were enhanced by low concentrations of magnesium.
Magnesium ions affect both presynaptic and effector sites in rabbit thoracic aortae but in a different manner; magnesium manifests only an inhibitory effect on noradrenaline release from the adrenergic nerves, but dual effects on reactivity of vascular smooth muscle, depending on concentrations of magnesium and stimulants; it is suggested that the change in vascular reactivity is more important than the reduction in transmitter release when magnesium inhibits the response to nerve stimulation.
EFFECTS OF SOME PYRAZINECARBOXAMIDES ON SODIUM TRANSPORT IN FROG SKIN
Authors: CUTHBERT A. W. , FANELL G. M. 
Published: July 2012

The inhibitory effect of amiloride (N‐amidino‐3,5‐diammo‐6‐chloropyrazinecarboxamide) on sodium transport in isolated skin of frog has been compared with 17 of its analogues. The dissociation constant of amiloride for passive sodium channels was 181.9 ± 8.9 nm, and the maximal percentage inhibition of sodium transport was 101.3 ± 0.4% (means of 123 measurements) when measured at a sodium concentration of 111 mm.
The N‐benzylamidino and N‐o‐chlorobenzylamidino compounds had affinities approximately 20 times larger than those for amiloride, and produced maximal inhibition of transport.
Substitution of chlorine in the 6‐position by other halogens showed that the bromo‐compound was equally active to amiloride, whereas the iodo derivative had an affnity equal to 15% of that for amiloride.
Substitution in the 5‐amino group in 10 compounds reduced the affinities to less than 1% of that of amiloride, without affecting their ability to produce complete inhibition of transport.
N‐Amidino‐3,5‐diaminopyrazinecarboxamide was unique in that it produced an unusual concentration‐response relationship.
EFFECTS OF PROSTAGLANDIN E2 AND A PROSTAGLANDIN ENDOPEROXIDE ANALOGUE ON NEUROEFFECTOR TRANSMISSION IN THE RAT ANOCOCCYGEUS MUSCLE
Authors: TIMIMI KHAWLA S. AL , BEDWANI J.R. , STANTON A.W.B. 
Published: July 2012

Investigations were made into the effects of prostaglandin E2 (PGE2) and a prostaglandin endo‐peroxide analogue (Upjohn compound U‐46619) on the responses of the rat anococcygeus muscle to field stimulation of the intrinsic sympathetic nerves, and to exogenous noradrenaline. The effects of PGE2 on responses to stimulation of intrinsic inhibitory nerves were also studied.
PGE2 (5.6 × 10−8 or 2.8 × 10−6mol/l) decreased motor (sympathetic) responses to field stimulation at all frequencies tested (2 to 24 Hz). The prostaglandin also reduced the inhibitory responses to field stimulation, seen when the tone of the preparation had been raised and its sympathetic innervation had been blocked by guanethidine. However, these inhibitory responses were also reduced by other spasmogens (carbachol and 5‐hydroxytryptamine) which, like PGE2, further increased the tone of guanethidine‐treated preparations.
At a concentration of 5.6 × 10−8 mol/1, PGE2 had no effect on responses to noradrenaline, whereas at a fifty‐fold higher concentration the prostaglandin potentiated these.
Unlike PGE2, U‐46619 (5.6 × 10−8 mol/1) greatly potentiated motor responses to field stimulation, at frequencies from 0.75 to 24 Hz. This effect did not represent a specific facilitation of sympathetic neurotransmission, as responses to carbachol and 5‐hydroxytryptamine, as well as to noradrenaline, were also potentiated.
The results are discussed in relation to the effects of prostaglandins and prostaglandin endoperox‐ides on neuroeffector transmission in other sympathetically innervated tissues. It is concluded that PGE2 inhibits sympathetic neurotransmission in the rat anococcygeus muscle by a prejunctional action, whereas the predominant effect of U‐46619 is direct excitation of the muscle. The effect of PGE2 on inhibitory responses to field stimulation may represent an interference with inhibitory neuroeffector transmission in this tissue, or may simply be a consequence of the spasmogenic action of the prostaglandin.
THE UPTAKE AND RELEASE OF [3H]‐2‐AMINO‐6,7‐DIHYDROXY1,2,3,4‐TETRAHYDRONAPHTHALENE (ADTN) BY STRIATAL NERVE TERMINALS
Authors: DAVIS A. , ROBERTS P.J. , WOODRUFF G.N. 
Published: July 2012

A study has been made of the uptake and release of [G‐3H]‐2‐amino 6,7‐dihydroxy‐1, 2,3,4‐tetra‐hydronaphthalene (ADTN) by crude striatal synaptosomes of the rat.
Uptake was rapid, temperature‐dependent and could be suppressed by a variety of metabolic inhibitors.
The Michaelis‐Menten kinetics indicated the presence of two distinct transport systems in the striatum which were of much higher capacity than those found in the cerebellum, which lacks dopaminergic innervation.
Uptake of [3H]‐ADTN was strongly inhibited by dopamine and the two potent dopamine‐uptake inhibitors, benztropine and nomifensine, but only weakly by imipramine and amphetamine (the latter in non‐reserpine‐treated animals).
Accumulated [3H]‐ADTN could be released from striatal slices by elevated K+. A similar release was evoked upon the addition of the ionophore, A23187.
The most potent releaser of [3H]‐ADTN was (+)‐amphetamine. This effect occurred at concentrations inactive against ADTN uptake. The neuroleptic ris‐flupenthixol produced an inhibition of the spontaneous release.
It is concluded that [3H]‐ADTN is accumulated preferentially into areas of the rat brain rich in dopamine. The pharmacological specificity of the uptake suggests that it is a good substrate for the dopamine carrier. Following uptake, [3H]‐ADTN may be released by K+ and a calcium ionophore, which raises the possibility that ADTN might act as a false transmitter.
THE EFFECT OF BACLOFEN ON α‐FLUPENTHIXOL‐INDUCED CATALEPSY IN THE RAT
Authors: DAVIES J.A. , WILLIAMS J. 
Published: July 2012

α‐Flupenthixol (α‐FPT; 0.2 mg/kg i.p.) when administered to rats produced catalepsy.
Baclofen (10 mg/kg i.p.) given 30 min after α‐FPT had a biphasic effect on the catalepsy. Initially there was a potentiation of the effect, followed by a significant attenuation of the degree of catalepsy.
Possible mechanisms of action are discussed.
ANTI‐DEPRESSANT ACTION OF CAESIUM CHLORIDE AND ITS MODIFICATION OF CHLORPROMAZINE TOXICITY IN MICE
Authors: MESSIHA F.S. 
Published: July 2012

Adult male mice were treated with caesium chloride (1.0 mEq/kg, i.p.) once daily for 54 consecutive days before administration of a single dose of reserpine (2.0 mg/kg) or (+)‐amphetamine (1.0 mg/kg). Pretreatment with caesium chloride resulted in potentiation of amphetamine‐produced enhancement of motility and in antagonism of reserpine‐induced behavioural depression in mice as measured by a locomotor activity test, compared to the respective controls.
Chronic administration of caesium chloride (1.0 mEq/kg daily) with gradual dose build‐up of chlorpromazine (up to 50 mg kg−1 day−1) counteracted chlorpromazine‐produced mortality in mice.
The results suggest an antidepressant property for Cs+ and the combined treatment of caesium chloride with chlorpromazine might have a clinical application, i.e. in the management of chlorpromazine‐induced adverse reactions.
RAT ISOLATED PHRENIC NERVE‐DIAPHRAGM PREPARATION FOR PHARMACOLOGICAL STUDY OF MUSCLE SPINDLE AFFERENT ACTIVITY: EFFECT OF OXOTREMORINE
Authors: GANGULY D.K. , NATH D.N. , ROSS H‐G. , VEDASIROMONI J.R. 
Published: July 2012

Muscle spindle afferent discharges exhibiting an approximately linear length‐frequency relation could be recorded from the phrenic nerve in the isolated phrenic nerve‐diaphragm preparation of the rat.
Muscle spindle afferent discharges could be identified by their characteristic ‘spindle pause’ during muscle contraction and by their response to succinylcholine.
Cholinergic influence on spontaneous and stretch‐induced afferent discharges was indicated by the augmentation produced by physostigmine and acetylcholine. (+)‐Tubocurarine, but not atropine, prevented this augmentation indicating the presence of curariform cholinoceptors in muscle spindles.
Acetylcholine did not appear to be involved in the genesis of spindle afferent discharges as incubation with hemicholinium‐3 and (+)‐tubocurarine failed to affect the rate of spontaneous and stretch‐induced spindle discharges.
Oxotremorine markedly increased the rate of spontaneous and stretch‐induced spindle afferent discharges and this effect was prevented in the presence of hemicholinium‐3 and (+)‐tubocurarine.
These results with oxotremorine are of interest in connection with the observation that muscle spindle afferents are hyperactive in Parkinsonian patients.
A COMPARISON OF DRUG‐INDUCED RESPONSES ON RAT TRACHEAL BRONCHIAL AND LUNG STRIP in vitro PREPARATIONS
Authors: BURNS J.W. , DOE J.E. 
Published: July 2012

A preparation of rat trachea and a new preparation of rat bronchi are described. Both preparations are fluid‐filled and the intraluminal pressure is monitored.
A preparation of rat peripheral airways, the lung strip, is described. The preparation consists of a thin strip of lung parenchyma which is supervised, and contractions monitored isotonically.
The rat trachea and bronchi have no intrinsic tone but increases in pressure are elicited in response to methacholine. The preparations relax in response to isoprenaline and aminophylline in the presence of a methacholine‐induced contraction. Both preparations respond weakly and show tachyphylaxis to 5‐hydroxytryptamine (5‐HT).
The lung strip contracts with equal magnitude to methacholine and 5‐HT. It exhibits intrinsic tone which is inhibited by indomethacin and relaxed by isoprenaline.
ENHANCEMENT OF A NOCICEPTIVE REACTION BY OPIOID ANTAGONISTS IN MICE
Authors: JACOB J.J.C. , RAMABADRAN K. 
Published: July 2012

The opioid antagonists, naloxone, GPA 2163, levallorphan and Mr‐2266 reduced the latency of the jumping reaction of mice in the hot plate test. The (+)‐isomers of levallorphan and Mr‐2266 which are devoid of antagonistic activity did not increase this latency.
In the same nociceptive reaction test, the enhancing effect of naloxone progressed in a dose‐range similar to that required for the antagonism by naloxone of the depressive action of morphine.
The facilitatory effect of naloxone was not blocked by the previous administration of morphine or etorphine but it was prevented by pretreatment with a high dose of buprenorphine.
The antagonism by naloxone of morphine and of buprenorphine did not follow the same pattern.
The factors which are or may be involved in the efficacy of naloxone in enhancing nociceptive reactions are discussed.
The enhancing effect of naloxone may be due to an antagonism of endogenous ligands for the opiate receptor. If so, these ligands would be involved in reaction to but not in perception of nociceptive stimuli which need not be harmful ones.
SELECTIVE EFFECTS OF MORPHINE ON THE NOCICEPTIVE RESPONSES OF THALAMIC NEURONES IN THE RAT
Authors: HILL R.G. , PEPPER CHRISTINE M. 
Published: July 2012

The effects of intravenous morphine on the firing of single sensory neurones in the thalamus of the anaesthetized rat are described.
Low doses (0.38 to 2.00 mg/kg) of morphine depressed the excitation of nucleus lateralis neurones produced by natural noxious stimuli but were without effect on spontaneous activity. The excitation of some of these neurones by iontophoretically applied acetylcholine or glutamate was also depressed by morphine. These effects were reversed by intravenous (0.25 to 1.17 mg/kg) but not iontophoretically applied (50 to 200 nA) naloxone.
Similar or higher doses of morphine (0.58 to 5.07 mg/kg) did not prevent the excitation of ventrobasal thalamic neurones by non‐noxious stimuli.
The possibility of a direct action of intravenous morphine in the thalamus is discussed.