bluuebunny/crossref_metadata_2025_split huggingface dataset:
The influence of drugs on the uptake of acetylcholine by slices of rat cerebral cortex
Authors: POLAK R. L. 
Published: July 2012

The acetylcholine content of cortical slices from rat brain, was determined after incubation for 30 min in a medium containing acetylcholine (4 μg/ml.). The cholinesterase activity of the slices had been inhibited by pretreatment with 3,3‐dimethyl‐n‐butyl 2‐methylphosphonofluoridate (soman).
Acetylcholine accumulated in the tissue slices, up to a concentration of about six times that in the medium.
The uptake of acetylcholine was partly inhibited by potassium in high concentrations.
Hemicholinium‐3, O‐ethyl S‐diethylaminoethyl ethylphosphonothiolate, physostigmine, atropine and choline, in that order of potency, inhibited the accumulation of acetylcholine in the cortical slices, but soman and ethyl N,N‐dimethyl phosphonoamidocyanate (tabun) had no effect on the uptake of acetylcholine.
Substances interfering with energy metabolism, such as 2,4‐dinitrophenol, oligomycin, sodium azide, amylobarbitone sodium and p‐chloromercuribenzoate inhibited the uptake of acetylcholine. Ouabain had little inhibitory effect.
In anaerobic conditions the accumulation of acetylcholine in the tissue slices was nearly blocked.
The uptake of acetylcholine in the tissue slices was dependent on temperature. The Q10 was about 2.
Autoradiography of sections from slices in which 3H‐acetylcholine had accumulated showed a diffuse distribution of radioactivity in the cytoplasm of all cells. There was no visible preference for certain cells or cell structures.
Regulation of metaraminol efflux from rat heart and salivary gland
Authors: COSTA E. , NEFF N. H. , NGAI S. H. 
Published: July 2012

The turnover rate of noradrenaline (NA) in heart and submaxillary salivary gland was studied in rats exposed to 4° C or maintained at room temperature (22° C). Cold exposure increased the turnover of the NA store in heart but not in salivary gland.
In another series of experiments the decline of metaraminol (M) from heart and submaxillary salivary gland was studied in rats exposed to 4° C or maintained at room temperature. Cold exposure accelerated the efflux of M from heart, but not from salivary gland. It is concluded that the accelerated decline of M from heart is the consequence of selective activation of the sympathetic nerves that innervate the heart.
The turnover of NA was studied in rat heart after the administration of M (100 μg/kg intravenously) or its precursor α‐methyl‐meta‐tyrosine (200 mg/kg intraperitoneally). Turnover remained essentially normal after these drugs.
The administration of desipramine (DMI, 20 mg/kg intraperitoneally) 1 hr after M (100 μg/kg intravenously) induced a rapid sustained efflux of M from heart and salivary gland. The results of this study suggest that the slow decline of M from heart is the result of the great affinity of the amine retrieval mechanism in sympathetic nerve endings for M. DMI inhibits the retrieval mechanism, thus accelerating the efflux of M.
The characteristics of acetylcholine release mechanisms in the auditory cortex
Authors: HEMSWORTH B. A. , MITCHELL J. F. 
Published: July 2012

The characteristics of the acetylcholine (ACh) release mechanism have been studied in the auditory cortex of rabbits on stimulation of the ipsilateral medial geniculate nucleus.
On stimulation of the medial geniculate nucleus the mean release of ACh from the auditory receiving cortex was 6.1 times the spontaneous release; the mean release from other parts of the cortex was 2.2 times the spontaneous release.
The frequency of stimulation most effective in evoking ACh release was found to be 10/sec.
Both the spontaneous and evoked release of ACh were reduced by 40–65% in the absence of calcium from the solution bathing the auditory cortex, and increased by 15–25% when the calcium concentration in the bathing solution was doubled.
The presence of low concentrations of magnesium in the fluid bathing the cortex was essential for the optimal release of ACh, but high magnesium concentrations lowered this release.
The presence of triethylcholine (TEC) in the fluid bathing the auditory cortex reduced both the spontaneous and evoked release of ACh. This reduction was reversed in the presence of choline.
The effects of calcium, magnesium and TEC on the ACh release mechanism in the cerebral cortex and at the neuromuscular junction are compared.
The pharmacology of salivary myoepithelial cells in dogs
Authors: EMMELIN N. , OHLIN P. , THULIN A. 
Published: July 2012

. Pressure changes in the submaxillary and parotid ducts of dogs, induced by nerve stimulation or intravenous injection of drugs, were studied.
. Pressure rises could be elicited by parasympathetic stimulation and by acetylcholine and methacholine, even when no secretion was evoked. These effects were abolished by atropine.
. Similarly, sympathetic stimulation, adrenaline, noradrenaline and phenylephrine raised the pressure in both glands, also in the absence of secretion. Dihydroergotamine abolished these effects. Isoprenaline increased the pressure in the submaxillary duct, but only when it caused secretion. This effect was abolished by propranolol. In the parotid gland isoprenaline caused neither secretion nor pressure rise. It is concluded that the myoepithelial cells of the two glands are supplied with α‐adrenoceptors.
. Doses of histamine, bradykinin, kallidin and physalaemin which caused no salivary secretion raised the duct pressure even when dihydroergotamine, propranolol and atropine had been given.
. Angiotensin and 5‐hydroxytryptamine increased the pressure only in some experiments. Oxytocin caused very little or no pressure rise. Vasopressin had no effect of its own but reduced the pressure raising effects of nerve stimulation or drugs.
Prostaglandins A1, A2 and 19‐hydroxy A1; their actions on smooth muscle and their inactivation on passage through the pulmonary and hepatic portal vascular beds
Authors: HORTON E. W. , JONES R. L. , HOPKIN JUDY M. , HORTON E. W. 
Published: July 2012

. Prostaglandins A1, A2 and 19‐hydroxy A1 have qualitatively similar actions to prostaglandin E1 on smooth muscle.
. The prostaglandins A have little activity on gastrointestinal, respiratory and reproductive smooth muscle but are potent depressors of the systemic arterial blood pressure of the dog, cat and rabbit.
. Our experiments support the view that the depressor action of the prostaglandins E and A is due to a direct dilator action on many peripheral vascular beds and not due to changes in nervous tone to these beds.
. A single passage through the pulmonary circulation of the cat or dog causes substantial loss of the vasodilator activity of prostaglandin E1 but little if any loss of the vasodilator activity of the prostaglandins A.
. A single passage through the hepatic portal circulation of the cat causes substantial loss of the vasodilator activity of prostaglandins E1, A1 and A2.
. The cat blood pressure and rat fundal strip would be a suitable combination for the parallel biological assay of the prostaglandins A1 and A2.
ACTH and decubitus ulceration: an experimental study
Authors: BARTON A. A. , BARTON MARY 
Published: July 2012

. Ulcers due to neurectomy with excision of the sciatic nerve are more severe than those due to tenotomy and can be inhibited by a single dose of ACTH.
. Timing and mode of administration of ACTH to prevent decubitus ulceration is critical and depends on its ability to prevent the separation of endothelial cells.
Role of catecholamines in centrogenic cardiac arrhythmia induced by aconitine
Authors: BHARGAVA K. P. , KOHLI R. P. , SINHA J. N. , TAYAL G. 
Published: July 2012

. Injection of 20 μg of aconitine into the lateral ventricle of dogs anaesthetized with pentobarbitone regularly induced cardiac irregularities and hypertension. The cardiovascular changes appeared within 5 min and lasted for about 90 min. Tachyphylaxis to the aconitine‐induced cardiovascular effects was observed.
. The aconitine‐induced arrhythmia and hypertension were centrogenic, for they were abolished or prevented by spinal transection (C2) or ganglionic blockade.
. Bilateral vagotomy as well as bilateral stellate ganglionectomy merely raised the threshold for arrhythmia without affecting the blood pressure response. The neural supply to the heart, therefore, does not seem to be the major pathway concerned in the genesis of the centrogenic cardiovascular effects of aconitine.
. The centrally evoked release of endogenous catecholamines from the adrenal glands was responsible for the aconitine‐induced arrhythmia, since the arrhythmia could be blocked or prevented by prior reserpinization, bilateral adrenalectomy or thoracic splanchnic nerve section.
. α‐ and β‐adrenoceptive receptor blocking agents prevented or abolished the aconitine‐induced arrhythmia in a manner similar to the catecholamine‐induced arrhythmia.
Microelectrode studies in the frog isolated spinal cord during depression by general anaesthetic agents
Authors: RICHENS A. 
Published: July 2012

. Extracellular and intracellular potentials have been recorded from the isolated spinal cord of the frog during depression of synaptic transmission by volatile and barbiturate general anaesthetic agents.
. Volatile agents did not impair conduction in presynaptic terminals in concentrations which completely blocked synaptic transmission.
. Methohexitone consistently impaired conduction in presynaptic terminals long before transmission through polysynaptic pathways was blocked.
. Volatile agents depressed the excitability of the motoneurone membrane, as evidenced by impaired antidromic invasion, reduced excitability to direct stimulation, depression of the synaptic potential and elevation of firing threshold. It is concluded that these actions are responsible for the depressant effect of volatile agents on spinal reflexes.
. Methohexitone produced an increase in the excitability of the motoneurone membrane, as evidenced by enhanced antidromic invasion, increased excitability to direct stimulation and potentiation of short latency responses. Despite this excitatory action, the polysynaptic pathways through the cord were depressed by an action of the drug on conduction in presynaptic terminals.
. It is suggested that the sensitivity of the motoneurone membrane to volatile agents may contribute to the good muscle relaxant properties of these drugs in clinical use.
Studies on the action of acetylcholine on the sino‐auricular node of the dog
Authors: DUTTA S. N. , SANYAL R. K. , TRIPATHI O. N. 
Published: July 2012

. The response of the sino‐auricular node to direct injection of acetylcholine in the artery supplying the node has been studied in the dog.
. Acetylcholine in graded doses (2, 5, 10 μg) caused acceleration of the sinus rhythm.
. The time course of the positive chronotropic action of acetylcholine resembled that produced by adrenaline or noradrenaline.
. The positive chronotropic action produced by acetylcholine was blocked by dichloro‐isopropylnoradrenaline and pronethalol and potentiated by cocaine.
. In reserpinized dogs, acetylcholine in similar doses produced sinus bradycardia. The positive chronotropic response could be temporarily restored by infusion of adrenaline or noradrenaline.
. Atropine blocked both the positive and negative chronotropic actions of acetylcholine.
Effect of reserpine on the subcellular distribution of 3H‐α‐methylnoradrenaline in the mouse heart
Authors: LUNDBORG P. 
Published: July 2012

. Mice were injected with reserpine (0.5 mg/kg or 2.5 mg/kg) at various intervals after an intravenous injection of 3H‐α‐methylnoradrenaline (3H‐α‐MeNa), 20 μg or 100 μg/kg. The effect of reserpine on the content of labelled amine in the subcellular fractions of the heart was studied.
. In most experiments reserpine caused a pronounced decrease in the 3H‐α‐MeNA content of the particulate fraction (P). The decrease was most pronounced when the higher dose of reserpine and lower dose of α‐MeNA were used. In most experiments, the 3H‐α‐MeNA content of the supernatant fractions was unchanged and, therefore, the P/(P + S) ratio was decreased.
. It is concluded that the effect of reserpine is a releasing effect on the particulate (granular) fraction, probably by blocking the re‐uptake of the amine leaked from the granules. No support was found for the hypothesis that reserpine acts by inhibition of release of amines from the nerve granules.
The uptake of cardiac glycosides by intestinal smooth muscle of the guinea‐pig in relation to digitalis receptors
Authors: GODFRAIND T. , LESNE M. 
Published: July 2012

Summary
. The accumulation and release of 3H‐digitoxin, 3H‐digoxin and 3H‐ouabain by isolated guinea‐pig intestinal smooth muscle has been studied and compared with a pharmacological action due to inhibition of the sodium pump.
. The uptake of labelled cardiac glycosides can be described by means of an exponential function. The t of uptake was similar for the three compounds and did not depend on the concentration.
. Analysis of the curve relating the uptake of cardiac glycosides at equilibrium to the bath concentration enabled a non‐saturable and a saturable binding site to be distinguished.
. In contrast to the uptake observations, the onset of the pharmacological effect was dependent on the concentration, and furthermore the t½; for this effect was shorter.
. The release of cardiac glycosides proceeded more slowly than the uptake.
. The uptake of a labelled glycoside was reduced in the presence of another glycoside. The amount of displaceable glycoside was nearly equivalent to the capacity of the saturable binding site.
. The significance of these results is discussed.
Pharmacological significance of biogenic amines in the lungs: 5‐hydroxytryptamine
Authors: SADAVONGVIVAD CHIRAVAT 
Published: July 2012

Summary
. A technique for the spectrofluorometric analysis of 5‐hydroxytryptamine, histamine, noradrenaline and dopamine in a single lung sample has been developed. The method is a combination of the extraction procedure of Shore & Olin (1958), plus the modification introduced by Hogans (1967) for the analysis of three of the four amines. The fourth amine, histamine, was analysed by the method of Shore, Burkhalter & Cohn (1959), which was combined with the analysis of the other three amines. The combined procedure consisted principally of disintegrating the lung tissue in butanol and subsequent separation of amines for measurement of fluorescence, either directly, as for 5‐hydroxytryptamine, or after formation of fluorophores, as for histamine, noradrenaline and dopamine. It has been possible to analyse all four amines from a sample of the lung in which the bronchopulmonary responses have been investigated.
. The concentration of 5‐hydroxytryptamine in the lung of seven species ranges from about 0·5 μg/g in the guinea‐pig, dog and man to about 7 μg/g in the rabbit. The pulmonary resistance is increased after an injection of 5‐hydroxytryptamine in the rat and guinea‐pig.
. The guinea‐pig is more sensitive to 5‐hydroxytryptamine than the rat. In both animal species, the content of 5‐hydroxytryptamine in the lung is elevated by administration of either 5‐hydroxytryptamine or 5‐hydroxytryptophan. In the rat, the administration of p‐chlorophenylalanine reduces the content of 5‐hydroxytryptamine in the brain but not in the lung.
. It is suggested that the 5‐hydroxytryptamine contained in the lung tissue is stored mainly in the platelets and in the mast cells.
A comparison of the cardiovascular actions of AQ 110 with those of isoprenaline and salbutamol
Authors: FOGELMAN F. , GRUNDY H. F. 
Published: July 2012

Summary
. AQ 110 is a β‐adrenoceptor agonist which, like isoprenaline and salbutamol, acts directly on the receptors.
. Compared with isoprenaline, AQ 110 has relatively stronger actions on bronchial and vascular smooth muscle (β2‐adrenoceptors) than stimulant effects on heart muscle (β1‐adrenoceptors). The β2‐selectivity of AQ 110 is, however, much less than that of salbutamol, mainly due to the weak cardiac actions of the latter.
. At doses which were equipotent in decreasing the bronchoconstrictor effect produced by a standard dose of 5‐hydroxytryptamine, AQ 110 had marginally less hypotensive action than salbutamol and considerably less than isoprenaline.
. Although AQ 110, unlike salbutamol, possesses a catechol group it was found not to be a substrate for catechol‐O‐methyl transferase and this is considered to account for its significantly prolonged action, compared with isoprenaline, in vivo.
Physiological and drug‐induced changes in the glycogen content of mouse brain
Authors: HUTCHINS D. A. , ROGERS K. J. 
Published: July 2012

Summary
. The effect of the method of killing on the concentration of glycogen in mouse brain was determined. The cerebral glycogen content of mice killed by immersion in liquid nitrogen did not differ significantly from that of animals decapitated and the heads immediately frozen. A delay before freezing led to the rapid loss of brain glycogen, with a 17% fall at 10 s and an 82% loss after 5 min.
. Hyperglycaemia, induced by the administration of d‐glucose, resulted in an 8.3% loss of brain glycogen after 120 min. Insulin hypoglycaemia produced a 10.7% fall in glycogen at 60 min followed by an 11.2% increase at 120 min.
. Exposure to either high (32° C) or low (10° C) ambient temperatures caused a depletion of brain glycogen.
. A circadian rhythm of brain glycogen concentration was found, with a nadir which was coincident with the peak of locomotor activity and body temperature.
. Drugs from several pharmacological classes were studied for their in vivo effect on the concentration of glycogen in mouse brain.
. Brain glycogen was increased by all the depressant drugs tested, and by some drugs which had little effect on behaviour (diphenhydramine, phenytoin and propranolol), or which caused excitation (caffeine and nialamide).
. Glycogen was depleted only by amphetamine‐like compounds or by bemegride‐induced convulsions.
. The results are discussed with particular reference to the possible relation between catecholamines and glycogen metabolism in the brain.
Pharmacology of some acetylcholine homologues
Authors: BARRASS B. C. , BRIMBLECOMBE R. W. , RICH P. , TAYLOR JOAN V. 
Published: July 2012

Summary
. The acetates of several long chain (3 to 12 methylene groups) analogues of choline have been prepared and their pharmacological properties studied.
. None of the compounds had a high level of activity at the post‐ganglionic parasympathetic acetylcholine receptors. The lower members of the series showed weak agonist activity and the homologues with 8 to 10 methylene groups had very weak anticholinergic activity.
. All the compounds had a depolarizing action at the acetylcholine receptors of the neuromuscular junction and of sympathetic ganglia. At the neuromuscular junction there were two peaks of stimulant activity, one with the hexamethylene and one with the dodecamethylene homologue, whereas at the ganglion there was only one peak, with the hexamethylene homologue.
. The ganglion‐stimulant activity of the higher members of the series was blocked by pretreatment with the anticholinesterase drug dyflos, whereas the activity of lower members was either unaffected by such treatment or slightly potentiated.
. The results are discussed in terms of possible spatial arrangements of acetylcholine receptor units in the neuromuscular junction and the ganglion.
Lack of antagonism between thioglycerol and an oxytocin analogue not containing a disulphide bond
Authors: SCHILD H. O. 
Published: July 2012

Summary
. The antagonistic effect of thioglycerol against oxytocin and an analogue of oxytocin not containing a disulphide bridge (desamino‐1‐carba‐oxytocin) has been compared in the rat isolated depolarized uterus.
. Thioglycerol clearly differentiated between the two compounds, 40 mm producing a dose ratio of 12 with oxytocin but only 1.5 with the carba compound.
. It was confirmed that thioglycerol produces no appreciable destruction of oxytocin in vitro.
. The mode of action of thiols in antagonizing specifically S–S polypeptides is discussed. It is concluded that they probably do not produce their effect either by inactivating receptors or by inactivating S–S polypeptides in solution. A possible mechanism is that thiols potentiate the destruction of S–S polypeptides at the receptor site.
Nonspecific supersensitivity of the guinea‐pig vas deferens produced by decentralization and reserpine treatment
Authors: WESTFALL D. P. , Burn J. H. 
Published: July 2012

Summary
. The sensitivity of the guinea‐pig vas deferens to noradrenaline, histamine, methylfurmethide and potassium was examined in vitro following decentralization and reserpine treatment.
. One day after decentralization or administration of reserpine (1.0 mg/kg daily) the sensitivity of the vas deferens was not increased. After 5 days' treatment the muscle was supersensitive to all four stimulants.
. The magnitude of the sensitivity increase to an individual drug was the same following both chronic reserpine treatment and decentralization. However, the degree of supersensitivity differed for the four stimulants. The order of potentiation was noradrenaline>histamine>methylfurmethide>potassium.
. The magnitude of the supersensitivity was inversely correlated with the slope of the dose‐response curves to the four agonists. The dose‐response curve to potassium had the steepest slope, followed in order by methylfurmethide, histamine and noradrenaline.
. A hypothesis is presented to account for the inverse relationship between the slope of the dose‐response curve and the degree of supersensitivity which follows reserpine treatment or decentralization.
Studies on the interrelationship between the syntheses of noradrenaline and metaraminol
Authors: JOHNSON G. E. , PUGSLEY T. A. 
Published: July 2012

Summary. Experiments were conducted to determine the influence of the rate of noradrenaline synthesis on the conversion of alpha‐methyl‐m‐tyrosine to metaraminol.. Male Wistar rats, 175–200 g, were placed into four groups and treated with (1) alpha‐methyl‐p‐tyrosine methyl ester, 250 mg/kg (2)dl‐alpha‐methyl‐m‐tyrosine, 400 mg/kg (3) alpha‐methyl‐p‐tyrosine methyl ester, 250 mg/kg plusdl‐alpha‐methyl‐m‐tyrosine, 400 mg/kg or (4) an equivalent volume of injection vehicle. All solutions were injected intraperitoneally.. Immediately after treatment half of the rats were transferred to 4° C with the remaining animals being kept at 27° C.. The rats were killed 4, 8 and 12 h after injection, the brains, hearts, spleens and adrenals removed and analysed for adrenaline, noradrenaline, metaraminol and alpha‐methyl‐m‐tyramine.. In virtually all cases, both during rest (27° C) and sympathetic stress (4° C), treatment of the rats with alpha‐methyl‐p‐tyrosine methyl ester increased the amount of metaraminol formed from alpha‐methyl‐m‐tyrosine. The only organ not containing increased quantities of metaraminol in the presence of alpha‐methyl‐p‐tyrosine methyl ester was the adrenals, taken from the rats kept at 27° C. Adrenals removed from the cold‐exposed rats contained more metaraminol when alpha‐methyl‐p‐tyrosine methyl ester was combined with alpha‐methyl‐m‐tyrosine than when alpha‐methyl‐m‐tyrosine was used alone.. These results demonstrate that the inhibition of noradrenaline synthesis, by treatment with the tyrosine hydroxylase inhibitor alpha‐methyl‐p‐tyrosine methyl ester, increased the conversion of alpha‐methyl‐m‐tyrosine to metaraminol. It is concluded that inhibiting the formation of dopa allowed increased amounts of alpha‐methyl‐m‐tyrosine to enter the biosynthetic pathway. These results support the false sympathetic transmitter concept advanced for metaraminol.