bluuebunny/crossref_metadata_2025_split huggingface dataset:
The relation of adenyl cyclase to the activity of other ATP utilizing enzymes and phosphodiesterase in preparations of rat brain; mechanism of stimulation of cyclic AMP accumulation by adrenaline, ouabain and Mn++
Authors: KATZ S. , TENENHOUSE A. 
Published: July 2012

Summary
The mechanism of stimulation of cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) accumulation by adrenaline and ouabain and the effect of Mn++substitution for Mg++ as the metal ion requirement of this system was studied in cell‐free preparations of adenyl cyclase from rat brain.
In the rat cerebral cortex preparation, substitution of Mn++for Mg++significantly increased cyclic AMP accumulation while significantly inhibiting adenosine triphosphate (ATP) and adenosine diphosphate (ADP) hydrolysis and adenosine 5′‐monophosphate (AMP) accumulation. In the synaptic membrane preparation, in the absence of NaF, the highest amount of ATP hydrolysis was obtained in tissue prepared with Mn++and incubated with Mg++; under these conditions cyclic AMP accumulation was equal to that produced under any other condition and significantly higher than that observed in the presence of Mg++prepared and Mg++incubated tissue.
Preparation and/or incubation of tissue with Mn++significantly reduced phosphodiesterase (PDE) activity compared to that observed in Mg++prepared tissue.
Adrenaline and ouabain both significantly increased cyclic AMP accumulation in the rat cerebral cortex preparation but did not inhibit ATP or ADP hydrolysis. In the synaptic membrane preparation, in the presence of 001 mm Ca++, adrenaline but not ouabain significantly increased cyclic AMP accumulation. Phenoxybenzamine (0·1 mm) and pronethalol (01 mm) significantly inhibited adrenaline‐induced cyclic AMP accumulation in both these preparations.
Ouabain and adrenaline both failed to stimulate cyclic AMP accumulation in the presence of Mn++prepared and/or incubated tissue.
Ouabain and adrenaline had no effect on PDE activity in either of these preparations.
It was concluded that Mn++increased cyclic AMP accumulation in part by indirect inhibition of ATP and ADP hydrolysis which provides inhibitors of cyclic AMP destruction, by direct stimulation of adenyl cyclase and by inhibition of cyclic AMP destruction in a way unrelated to nucleotide inhibition of PDE. Adrenaline and ouabain appeared to stimulate cyclic AMP accumulation in a more direct manner.
Pentobarbitone inhibition of catecholamine secretion
Authors: HOLMES J. C. , SCHNEIDER F. H. 
Published: July 2012

Summary
The perfused isolated cow adrenal gland was used to investigate the effect of barbituric acid, phenobarbitone and pentobarbitone on catecholamine secretion.
Pentobarbitone reduced catecholamine secretion induced by a number of drugs which cause exocytosis. The concentration of pentobarbitone which caused a 50% inhibition of catecholamine secretion was for acetylcholine 5·6 × 10−5m, for carbachol 6·3 × 10−5m, for histamine 1·6 × 10−4m, for (+)‐amphetamine 4·4 × 10−5m and for potassium chloride 1·5 × 10−4m. The degree of inhibition by pentobarbitone was not dependent on the concentration of the secretagogue.
Pentobarbitone (up to 10−3m) did not inhibit the catecholamine release that was induced by acetyldehyde or by calcium chloride; it inhibited slightly (34%) the catecholamine secretion induced by tyramine.
Catecholamine release induced by carbachol was also inhibited by phenobarbitone (50% inhibition at 2·8 × 10−4m (n = 7)) but was unaffected by barbituric acid.
Pentobarbitone had no effect on spontaneous or on (+)‐amphetamine‐ or tyramine‐induced release of catecholamines from isolated chromaffin vesicles of cow adrenal medulla.
It is concluded that pentobarbitone inhibits catecholamine release by preventing a configurational change in the structure of the membrane of the chromaffin cell which is a necessary link between receptor activation and catecholamine release.
Release of rabbit aorta contracting substance (RCS) and prostaglandins induced by chemical or mechanical stimulation of guinea‐pig lungs
Authors: PALMER M. A. , PIPER PRISCILLA J. , VANE J. R. 
Published: July 2012

Summary
Rabbit aorta contracting substance (RCS) and prostaglandins were released from guinea‐pig isolated perfused lungs by gentle massage and also by infusion of Prosparol.
RCS and prostaglandins were also released by infusion into the pulmonary artery of bradykinin, arachidonic and dihomo‐γ‐linolenic acids or shock perfusate (containing RCS‐releasing factor).
Arachidonic and dihomo‐γ‐linolenic acids caused a prolonged release of RCS and prostaglandins whereas bradykinin and shock perfusate gave a short‐lasting output.
RCS and prostaglandins, together with histamine were released when super‐fused chopped lung tissue was agitated.
Challenge of sensitized guinea‐pigs in vivo led to the release of an RCS‐like substance into the carotid arterial blood.
Intravenous injection of bradykinin into guinea‐pigs also released an RCS‐like substance.
The release of RCS and prostaglandins was inhibited by aspirin or indomethacin in all experiments.
RCS contracted all vascular tissues investigated and also rat stomach strip.
The half‐life of RCS was estimated as 1–2 minutes.
Decreased synthesis of DNA in regenerating rat liver after the administration of reserpine
Authors: ĆIHÁK A. , VAPTZAROVA K. 
Published: July 2012

Summary
Reserpine given to rats before the enhanced synthesis of DNA begins 14h after partial hepatectomy markedly depresses thymidine uptake into DNA at 24 hours.
At this time decreased activity of liver thymidine kinase but unchanged thymidine 5′‐nucleotidase were observed.
Reserpine has no effect on DNA synthesis when administered simultaneously with the labelled thymidine 2 h before killing.
With depressed DNA synthesis after reserpine administration there is no significant decrease of liver RNA synthesis.
[3H]‐adenine nucleotide and [3H]‐noradrenaline release evoked by electrical field stimulation, perivascular nerve stimulation and nicotine from the taenia of the guinea‐pig caecum
Authors: KUCHII M. , MIYAHARA J. T. , SHIBATA S. 
Published: July 2012

Summary
The release of [3H]‐noradrenaline and adenine nucleotide evoked by electrical field stimulation (20–60 V, 30 Hz), perivascular nerve stimulation (20–80 V, 60 Hz) and nicotine (10, 100 μm) was studied in the taenia of the guinea‐pig caecum under various conditions.
Electrical stimulation at high intensity (60 V) caused the release of [3H]‐adenine nucleotide; however, the inhibitory action of electrical stimulation was proportional to [3H]‐noradrenaline release.
The intensity of the inhibitory effect of stimulation of the perivascular nerves was directly related to [3H]‐noradrenaline release and not associated with the release of [3H]‐nucleotide.
Cold storage for more than 8 days, cooling (19° C) or tetrodotoxin treatment (1 μg/ml) abolished the inhibitory responses to electrical stimulation and to nicotine. After these treatments, nicotine and electrical stimulation elicited only contractions; the release of [3H]‐noradrenaline, but not that of [3H]‐adenine nucleotide, was inhibited.
The dissociation of the inhibitory effects of electrical stimulation and nicotine from [3H]‐nucleotide release does not support the hypothesis that ATP or a related nucleotide is the humoral transmitter of the non‐adrenergic inhibition in the taenia of the guinea‐pig caecum.
Inhibition by diuretics of cyclic 3′,5′‐AMP‐dependent protein kinase from toad bladder epithelium
Authors: FERGUSON D. R. , TWITE B. R. 
Published: July 2012

Summary
A cAMP‐dependent protein kinase enzyme has been isolated from toad bladder epithelium.
This enzyme catalyses the phosphorylation of histones; a reaction stimulated by 0·1 μm cAMP.
Activity of this enzyme in the presence of 01 μm cAMP was significantly inhibited by 100 μm mercuderamide, bumetanide and frusemide. A small, though statistically insignificant inhibition was seen with the same concentrations of hydrochlorothiazide and ethacrynic acid.
The half maximal inhibition was achieved with mercuderamide, 5 μm, and with frusemide and bumetanide 600 μm.
Interaction of (+)‐amphetamine with cerebral dopaminergic neurones in two strains of mice, that show different temperature responses to this drug
Authors: CACCIA S. , CECCHETTI G. , GARATTINI S. , JORI A. 
Published: July 2012

Summary
(+)‐Amphetamine sulphate elicits a dose‐dependent hyperthermia in NMRI mice but it does not significantly increase the body temperature of C3H mice.
When low doses of (+)‐amphetamine are given, the body temperature of C3H mice decreases.
(+)‐Amphetamine decreases the noradrenaline concentration in the brainstem and increases the homovanillic acid concentration (HVA) in the striatum of NMRI mice, but only slightly reduces the noradrenaline concentration and does not change the HVA concentration in the brains of C3H mice.
The two strains appear to show a difference in the metabolism of dopamine in the striatum. The rates at which dopamine disappears from the tissue after blocking catecholamine synthesis with α‐methyltyrosine and the rates at which HVA accumulates after blocking the active transport of this metabolite out of the brain with probenecid suggest that the turnover of dopamine is lower in C3H mice than in NMRI mice.
The role of sodium pump in the inhibition of smooth muscle responsiveness to agonists during potassium restoration
Authors: BOSE D. , INNES I. R. 
Published: July 2012

Summary
Isometric contractions of cat splenic capsular smooth muscle in response to noradrenaline and histamine were recorded.
Removal of potassium from the bathing medium did not change the resting tension or the responsiveness to noradrenaline. Restoration of potassium inhibited responses to noradrenaline or histamine only if the muscles were stimulated with an agonist while in the K‐free medium.
This inhibition of responses to the agonists due to potassium was reversed rapidly by removing the ion or reversed slowly by prolonged exposure to the ion. The inhibition was also blocked by procedures or agents which block the sodium pump (ouabain, substitution of NaCl by LiCl), inhibit active processes (low ambient temperature) or prevent intracellular accumulation of sodium (substitution of choline for sodium).
It is proposed that under special circumstances such as when there is an increase in internal sodium concentration, the sodium pump is probably electrogenic and causes relaxation when activated by external potassium. In the normal muscle the pump is probably electrically neutral.
The effects of drugs on the sensitivity of the rat anococcygeus muscle to agonists
Authors: GIBSON A. , POLLOCK D. 
Published: July 2012

Summary
The effects of cocaine, 6‐hydroxydopamine (6‐OHDA), reserpine and 17‐β‐oestradiol on the sensitivity of the rat anococcygeus muscle to noradrenaline (NA), acetylcholine (ACh) and KCl were investigated.
Cocaine (10−5m) increased the sensitivity of the anococcygeus to NA (100‐fold) but not to ACh or KCl.
6‐OHDA treatment, whether discontinuous over 6 days or continuous for 12 days, also produced a specific increase in sensitivity to NA (50‐fold).
Reserpine ((1 mg/kg)/day) produced a small increase in sensitivity of the muscle to NA and ACh but not to KCl, after 6 days and 12 days treatment.
17‐β‐Oestradiol (10–5m) had no effect on the sensitivity of the anococcygeus to NA or ACh, but reduced the sensitivity to KCl and the possible mechanism of this effect is discussed.
Cocaine increased, while reserpine, 6‐OHDA and 17‐β‐oestradiol decreased, the maximum response of the muscle to KCl. The response to KCl was shown to consist of at least three components; a direct action on the muscle, an effect due to release of NA, and an inhibitory action, probably due to release of the unknown inhibitory transmitter.
Mechanisms contributing to barbiturate intolerance in rats
Authors: ASTON R. 
Published: July 2012

Summary
Female rats, 3 weeks after pretreatment with 200 or 400 (mg/kg)/day barbitone for 2 or 30 days, exhibited a prolonged sleeping time and a reduced awakening barbiturate brain level when challenged with either barbitone or pentobarbitone. After 3 additional weeks, the latter responses had returned, or were returning to, control values.
Barbitone pretreatment schedules had no residual effect upon in vitro hepatic pentobarbitone‐metabolizing activity measured 3 or 6 weeks later, except in one instance, when hepatic enzyme activity was significantly enhanced 3 weeks after 30 daily doses of 200 mg/kg barbitone. In this case, however, an enhanced barbiturate sleeping time, together with a reduced awakening barbiturate brain level, were observed.
It is concluded that barbitone administered intraperitoneally in doses of 200 to 400 (mg/kg)/day for 2 or 30 days induces a non‐hepatogenic intolerance to barbiturates, related to an increased sensitivity of the central nervous system to these drugs. This central intolerance is seen 3 weeks, but not 6 weeks, after pretreatment. Furthermore, this central intolerance has been observed to co‐exist with an hepatic tolerance, a situation which could result in a reduced LD50 coupled with an increase in ED50.
A STUDY OF THE FACTORS AFFECTING THE SLEEPING TIME FOLLOWING INTRACEREBROVENTRICULAR ADMINISTRATION OF PENTOBARBITONE SODIUM: EFFECT OF PRIOR ADMINISTRATION OF CENTRALLY ACTIVE DRUGS
Authors: STEVENSON I.H. , BULL M.J. TURN 
Published: July 2012

Injection of pentobarbitone sodium into a lateral cerebral ventricle of rats produced a loss of righting reflex. The duration of anaesthesia was dose‐dependent.
The optimum dose of pentobarbitone to allow study of the factors affecting the sleeping time was considered to be 650 μg injected in 25 μl water.
In a study of the effect of age and sex on the sleeping time, the youngest rats used (88 g body weight) were found to be the most sensitive to barbiturate. Female rats were more sensitive than male animals.
The duration of anaesthesia was not affected by induction or inhibition of hepatic drug‐metabolizing enzyme activity.
Prior administration (acute) of central nervous system depressant drugs shortened the latent period and prolonged the duration of sleep. Prior administration of stimulant drugs antagonized the effect of pentobarbitone.
Animals withdrawn following chronic administration of a number of drugs, barbitone, barbitone/bemegride mixture, Mandrax (methaqualone: diphenhydramine; 10: 1), chlordiazepoxide, nitrazepam, chlorpromazine or ethanol, exhibited a significant tolerance to intracerebroventricularly administered pentobarbitone.
Withdrawal of amphetamine, morphine, methyprylon or diazepam did not result in tolerance to intracerebroventricularly administered pentobarbitone.
Chronic administration of all drugs except amphetamine and morphine induced a tolerance to intraperitoneally administered hexobarbitone (100 mg/kg).
The usefulness of sleeping time determination following intracerebroventricular administration of pentobarbitone as an assessment of central nervous system excitability is discussed. It is concluded that this method gives a valid indication of the sensitivity of the central nervous system to barbiturate and of the level of excitability in general. The method is particularly applicable in situations where the activity of hepatic drug‐metabolizing enzyme activity may be altered.
DISTRIBUTION OF α‐ AND β‐ADRENOCEPTORS IN HUMAN URINARY BLADDER
Authors: AWAD S.A. , BRUCE A.W. , CARRO‐CIAMPI G. , DOWNIE J.W. , LIN M. , MARKS G.S. 
Published: July 2012

The distribution of α‐ and β‐adrenoceptors in isolated preparations of human bladder neck and detrusor muscle has been studied.
Adrenaline caused contraction of the bladder neck which was blocked by phenoxybenzamine but unaltered by propranolol.
Isoprenaline caused relaxation of the bladder neck which was blocked by propranolol. High concentrations caused contraction which was enhanced by propranolol but blocked by phenoxybenzamine.
Detrusor muscle was relaxed by isoprenaline and this effect was blocked by propranolol. Phenylephrine caused relaxation of detrusor which was unaffected by phenoxybenzamine; in some cases contraction was produced in the presence of propranolol.
It is concluded that the bladder neck contains mainly α‐receptors and the detrusor mainly β‐receptors but both regions possess both types of adrenoceptor.
INHIBITION BY NON‐STEROID ANTI‐INFLAMMATORY AGENTS OF RABBIT AORTA CONTRACTING ACTIVITY GENERATED IN BLOOD BY SLOW REACTING SUBSTANCE C
Authors: FERREIRA S.H. , VARGAFTIG B.B. 
Published: July 2012

A crude and a partially purified preparation of slow reacting substance C (SRS‐C) as well as arachidonic acid decreased resistance to perfusion of the dog hind paw. This effect was suppressed by treatment with non‐steroid anti‐inflammatory drugs.
Injections of SRS‐C or of arachidonic acid induced marked and reproducible contractions of strips of rabbit aorta and a rat stomach which were bathed in blood from an anaesthetized dog. The effect on the rabbit aorta is attributed to formation of a rabbit aorta contracting substance (RCS). The contractions were suppressed when the dog was treated with a non‐steroid anti‐inflammatory drug.
Incubation of blood or of platelet‐rich plasma with SRS‐C or arachidonic acid resulted in the formation of similar materials. This formation was suppressed by anti‐inflammatory drugs.
SRS‐C, linoleic, linolenic, and arachidonic acids are suitable substrates for soybean lipoxidase for the generation of RCS.
It is suggested that RCS and prostaglandin are formed within platelets, when SRS‐C or arachidonic acid are injected into animals or added in vitro. Non‐steroid anti‐inflammatory drugs suppress these effects, possibly by inhibiting prostaglandin synthetase.
THE ACCUMULATION OF ADENOSINE IN RABBIT INTESTINAL MUSCLE
Authors: HULME MARILYN E. , WESTON A.H. 
Published: July 2012

Strips of longitudinal muscle from rabbit intestine accumulated radioactivity when exposed to [3H]‐adenosine.
Accumulation of radioactivity was not sodium‐dependent or ouabain‐sensitive, but was reduced by cooling, zero glucose plus bubbling with N2, 2,4, dinitrophenol, dipyridamole, hexobendine and lidoflazine.
After 7 min exposure to [3H]‐adenosine, the tissue was found to contain radioactive adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and adenosine itself in the approximate ratio 13: 6: 4: 1.
In the presence of dipyridamole, hexobendine or lidoflazine (each 1 μm), the amounts of radioactive ATP, ADP, AMP and adenosine were reduced with the concentration of adenosine not significantly different from controls.
It is concluded that energy‐dependent uptake of adenosine does not occur in the longitudinal muscle of rabbit intestine. Adenosine enters the tissue by a passive process and rapidly becomes phosphorylated giving rise to apparently high tissue: medium ratios.
The drugs dipyridamole, hexobendine and lidoflazine appear to reduce the accumulation of radioactivity by preventing the formation of adenosine phosphate derivatives.
THE HYPOGLYCAEMIC EFFECT OF 5‐HYDROXYTRYPTOPHAN
Authors: FURMAN B.L. 
Published: July 2012

In nialamide‐treated mice, L‐5‐hydroxytryptophan produced a dose‐dependent hypoglycaemic response which was independent of whether the animals had been fed or fasted.
This response was accompanied by a head‐twitching response which was also dose‐dependent.
The hypoglycaemic response was not accompanied by an elevation in plasma immunoreactive insulin levels and was fully manifest in alloxan diabetic animals.
5‐Hydroxytryptophan did not increase the in vitro glucose uptake of adipose tissue or skeletal muscle, either on incubation of the tissues in contact with the drug or on incubation of tissues removed from mice injected with the drug.
Both the hypoglycaemic and head‐twitching responses were prevented by pretreatment with methysergide or cyproheptadine and augmented by mepyramine treatment.
THE CARDIOVASCULAR EFFECTS OF INTRAVENTRICULAR CLONIDINE AND BAY 1470 IN CONSCIOUS HYPERTENSIVE CATS
Authors: FINCH L. 
Published: July 2012

Intraventricular administration of clonidine (5–30 μg) and an analogue, BAY 1470 (15–30 μg) to conscious renal hypertensive cats produced a fall in mean blood pressure lasting for approximately 3 hours. This fall in blood pressure was accompanied by a marked bradycardia.
Pretreatment with intraventricular phentolamine (100–200 μg), piperoxan (40–200 μg) or tolazoline (75–200 μg) abolished the cardiovascular effects of intraventricular clonidine (20 μg).
The cardiovascular effects of intraventricular clonidine (20 μg) were not modified by the pretreatment with either haloperidol (1 mg/kg i.p.) or desmethylimipramine (1 mg/kg i.p.).
Emesis was observed 1–2 min after the administration of either clonidine (5–20 μg) or BAY 1470 (30 μg). This preceded the cardiovascular actions and was still seen after pretreatment with haloperidol, desmethylimipramine, phentolamine, piperoxan or tolazoline.
It is concluded that the centrally mediated cardiovascular responses observed after intraventricular administration of small doses of clonidine are due to stimulation of central α‐adrenoceptors and are independent of central catecholamine uptake mechanisms and dopamine receptors.
EFFECTS OF IMIPRAMINE AND DESIPRAMINE ON RESPONSES OF SINGLE CORTICAL NEURONES TO NORADRENALINE AND 5‐HYDROXYTRYPTAMINE
Authors: BRADSHAW C.M. , ROBERTS M.H.T. , SZABADI E. 
Published: July 2012

The technique of microelectrophoresis was used in order to study the effects of imipramine and desipramine on single neurones in the somatosensory cortex of the cat, anaesthetized with halothane.
Imipramine and desipramine, when applied for a brief period, did not affect the firing rate of the vast majority of the neurones tested.
Both potentiation and antagonism of excitatory responses to noradrenaline could be observed after a brief application of either of the antidepressants. Four drug‐interaction patterns could be distinguished: potentiation of immediate onset; potentiation reaching its maximum after a delay; antagonism followed by potentiation; antagonism followed by recovery.
When different doses of the same antidepressant were applied, it was found that the drug‐interaction patterns were related to the dose of antidepressant applied, a lower dose causing potentiation, and a higher dose antagonism of the response.
Both potentiation and antagonism of depressant responses to noradrenaline could be observed.
Both excitatory and depressant responses to 5‐hydroxytryptamine were modified by imipramine and desipramine: a smaller dose of the antidepressant potentiated, and a higher dose antagonized the responses.
Excitatory responses to glutamate were not affected by imipramine and desipramine.
EFFECT OF CONVERTING ENZYME BLOCKADE ON ISOPRENALINE‐ AND ANGIOTENSIN I‐INDUCED DRINKING
Authors: HERTTING G. , MEYER D.K. 
Published: July 2012

Intravenous infusion of 0.072 μmol kg−1 h−1 (1‐Asp, 5‐Ile) angiotensin I, 0.116 μmol kg−1 h−1 of (1‐Asp β‐amid, 5‐Val) angiotensin II or of (1‐Asp, 5‐Ile) angiotensin II, caused food‐deprived and water‐satiated rats to drink about 3.0 ml of water per animal. This indicates that angiotensin I has a 1.6 times stronger dipsogenic effect than the angiotensin II preparations when infused intravenously.
The converting‐enzyme‐inhibitor SQ 20881 (Pyr‐Trp‐Pro‐Arg‐Pro‐Gln‐Ile‐Pro‐Pro) (1.0 mg/kg i.v.) had no intrinsic dipsogenic effect.
SQ 20881 given in combination with angiotensin I or angiotensin II potentiated the dipsogenic effect of angiotensin I, but not that of the two angiotensin II preparations.
The drinking induced by isoprenaline (100 μg/kg, i.m.) was potentiated by SQ 20881 to the same extent as drinking produced by angiotensin I infusion.
Angiotensin I plasma levels were determined after angiotensin I infusion and isoprenaline application. Both were significantly raised by SQ 20881.
It is concluded that one of the mechanisms which mediate the dipsogenic effect of isoprenaline is stimulation of the renin‐angiotensin system and that increased plasma levels of angiotensin I may play a substantial role in this type of drinking.