bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoamine oxidase in rat arteries: evidence for different forms and selective localization
Authors: COQUIL J. F. , GORIDIS C. , MACK G. , NEFF N. H. 
Published: July 2012

Summary
Two forms of monoamine oxidase activity were differentiated in rat mesenteric and femoral artery by means of substrate and inhibitor specificities: one form deaminated tyramine, 5‐hydroxytryptamine and noradrenaline and was highly sensitive to pargyline and clorgyline but resistant towards carbonyl reagents. This form resembled type A monoamine oxidase previously described. The other deaminated tyramine but not 5‐hydroxytryptamine or noradrenaline and was inhibited by carbonyl reagents but not by clorgyline or pargyline.
About one third of the total monoamine oxidase in homogenates of rat mesenteric artery was recovered in a 105 g supernatant. Both forms were partially soluble, but relatively less of the type A activity was recovered in the soluble fraction.
Chemical sympathectomy with 6‐hydroxydopamine resulted in a loss of 59% of monoamine oxidase activity in the mesenteric artery. There was a selective loss of type A activity, as revealed by the 70% decrease in 5‐hydroxytryptamine deaminating ability and by the marked decrease in clorgyline sensitivity. The second monoamine oxidase species was resistant to 6‐hydroxydopamine. The soluble activity was not affected by chemical sympathectomy. Most of the transmitter‐specific monoamine oxidase of the arterial wall was localized within the adrenergic nerve endings. Our observations are consistent with the hypothesis that extraneuronal monoamine oxidase plays only a minor role in metabolizing noradrenaline in sympathetically innervated tissues.
Plasma amine oxidase might originate from the arterial wall since it has similar characteristics to that found in the mesenteric artery.
The oestrous cycle and monoamine oxidase activity
Authors: HOLZBAUER MARGARETHE , YOUDIM M. B. H. 
Published: July 2012

Summary
During the oestrous cycle of the rat, monoamine oxidase (MAO) activity was studied in the uterus, the ovaries and the adrenal glands and also in 4 brain regions which are rich in monoamines. In all these structures the activity was lowest during the night between oestrus and metoestrus. High values were found in di‐oestrus, with the exception of the uterus in which the MAO activity reached its peak during metoestrus.
A stimulating effect of progesterone on uterine, ovarian and adrenal MAO activity was observed.
An index for the cyclic variations in progesterone production was obtained by measuring the adrenal and ovarian progesterone content at the same stages of the cycle as MAO activity.
The sum of the amounts of progesterone contained in the ovaries and adrenal glands was low in early oestrus but increased during late oestrus when MAO activity was at its minimum. Progesterone contents were high in met‐and di‐oestrus when MAO activity was also high.
Effects of intracoronary infusions of acetylcholine and nicotine on the dog heart in vivo
Authors: ROSS G. 
Published: July 2012

Summary
In anaesthetized dogs intracoronary infusions of high doses of nicotine and acetylcholine increased myocardial contractile force and this could be prevented by pre‐treatment with desmethylimipramine or phenoxybenzamine.
The inotropic effect of nicotine was brief and subsided during the continuing infusion of the drug. The infusion of nicotine did not reduce the inotropic effects of cardiac sympathetic nerve stimulation.
The inotropic effect of intracoronary acetylcholine often fluctuated during prolonged infusions and was not altered by pretreatment with atropine. Acetylcholine infusions reduced the inotropic responses produced by cardiac sympathetic nerve stimulation and led to a substantial transient reduction in the associated pressor responses. Intracoronary acetylcholine also reduced the pressor and inotropic effect of intravenous noradrenaline. The attenuation of these adrenergic cardiovascular responses by acetylcholine was prevented by atropine.
Passage of gallamine from blood into the liquor space in man and in dog
Authors: HARANATH P. S. R. K. , KRISHNAMURTY A. , RAO L. N. , SESHAGIRIRAO K. 
Published: July 2012

Summary
Patients receiving an intravenous injection of 2–3·8 mg/kg gallamine showed gallamine‐like activity in their lumbar c.s.f. collected 15 and 70–100 min after the injection. The activity assayed on acetylcholine contractions of frog rectus muscle was equivalent to between 0·1 and 0·75 μg/ml gallamine.
In anaesthetized dogs an intravenous injection as well as an intravenous infusion of gallamine led to the appearance of gallamine‐like activity in the cisternal c.s.f. and, on perfusion of the cerebral ventricles, in the effluent collected from the cisterna magna.
After an intravenous injection of 1 mg/kg the activity in the cisternal c.s.f. corresponded to between 0·2 and 1 μg/ml and in the effluent to between 130 and 175 ng/min during the first 15 min perfusion and then declined.
On intravenous infusion of gallamine at a rate of 10 (μg/kg)/min for 2 h the cisternal c.s.f. showed a uniform gallamine‐like activity corresponding to between 0·4 and 0·67 μg/ml during the infusion. In the cisternal effluent the gallamine‐like activity rose initially to between 20 and 90 ng/min but declined before the infusion was ended.
The intravenous injection of gallamine caused respiratory paralysis but did not affect arterial blood pressure; its intravenous infusion caused no respiratory paralysis and did not affect arterial blood pressure.
Predictions of the antimalarial activity of arylamidinoureas
Authors: GOODFORD P. J. , NORRINGTON F. E. , RICHARDS W. H. G. , WALLS L. P. 
Published: July 2012

Summary
Regression equations were calculated relating the observed antimalarial potencies of arylamidinoureas to their predicted physicochemical properties.
A two‐parameter equation was used to forecast the antimalarial activity of more arylamidinoureas.
Thirteen compounds of the predicted type were synthesized, and their observed antimalarial potencies compared with the forecasts.
Morphine‐tolerant longitudinal muscle strip from guinea‐pig ileum
Authors: GOLDSTEIN A. , SCHULZ R. 
Published: July 2012

Summary
Implantation of morphine pellets in guinea‐pigs produced a high degree of tolerance and dependence within 3 days.
The contractions of the longitudinal muscle induced by electrical stimulation of the myenteric plexus‐longitudinal muscle preparations obtained from tolerant animals were less depressed by morphine than the contractions evoked in preparations from non‐tolerant animals.
Naloxone did not alter the size of the evoked twitch but antagonized the depressant action of morphine in tolerant and in non‐tolerant animals. When given to tolerant guinea‐pigs, naloxone caused an increase in intestinal activity in vivo.
The contractile response of the longitudinal muscle to acetylcholine was the same in preparations obtained from tolerant and non‐tolerant animals. Electrically evoked contractions of the myenteric plexus‐longitudinal muscle preparations from tolerant animals showed reduced sensitivity to the depressant effects of adrenaline, isoprenaline, and particularly, dopamine.
Further studies regarding the structure activity relationships of β‐adrenoceptor antagonists
Authors: BAGWELL E. E. , WILLIAMS E. M. VAUGHAN 
Published: July 2012

Summary
The ortho (M66,527) and para (M66,368) analogues of 1‐t‐butylamino‐3‐(methoxyphenoxy)‐2‐propanol and para substituted tertiary butylphenoxy‐1‐N‐isopropylamine‐3 propanol‐2 oxalate acid (L8429) were tested in dogs for their β‐adrenoceptor blocking activity.
M66,527, which contains a methoxy group in the ortho position of the benzene ring, was found to be comparable to propranolol in blocking cardiac and peripheral vascular responses to isoprenaline. Like propranolol, M66,527 was more potent on peripheral receptors.
Transference of the methoxy group to the para position (M66,368) reduced the overall potency; however, this compound was found to be relatively cardioselective in that it was 2 to 3·6 times more active in blocking cardiac responses to isoprenaline.
The cardioselective properties of the short chain para methoxy substituent were less than those reported for compounds with longer para substitutions (i.e. practolol, para oxprenolol and para alprenolol).
L8429, with a tertiary butyl group in the para position, was a weak β‐adrenoceptor antagonist without cardioselective properties. A longer, less bulky n‐butyl group may provide for a more potent and selective antagonist.
The results support the view that the size and site of the substituent on the benzene ring may be of importance in determining the cardioselective potency of β‐adrenoceptor antagonists.
Delayed manifestation of ultraviolet reaction in the guinea‐pig caused by anti‐inflammatory drugs
Authors: GUPTA N. , LEVY L. 
Published: July 2012

Summary
Exposure of depilated skin of guinea‐pig to ultraviolet (u.v.) light for 20 s produces a prolonged inflammatory response.
The erythaema becomes evident within 15–30 min after the exposure and progressively increases in intensity reaching its maximum by 4–6 hours. The erythaema persists over 24 hours.
Increase in vascular permeability is biphasic with an early short‐lived rise peaking at 0·5 h and a prolonged secondary response peaking at 9–12 h and lasting over 48 hours.
In presence of aspirin, phenylbutazone and indomethacin, administered prior to u.v. exposure, the inflammatory reaction is partially suppressed, depending upon the dose. The drugs are ineffective in aborting or minimizing the response when given after the inflammation is established. Corticosteroids fail to influence the u.v. inflammation in this test. The significance of these findings is discussed.
A comparison of the effects of chemical sympathectomy by 6‐hydroxydopamine in newborn and adult rats
Authors: FINCH L. , HAEUSLER G. , THOENEN H. 
Published: July 2012

Summary
The effects of chemical sympathectomy with 6‐hydroxydopamine (6‐OHDA) on the cardiovascular system of the rat were compared in, (a) 10‐week‐old rats treated during the first 14 days after birth with 150 μg/g subcutaneously, and (b) adult rats injected intravenously with 2 × 50 mg/kg on day 1 and 2 × 100 mg/kg on day 7 and the experiments performed on day 8.
Intravenous administration of 6‐OHDA to adult rats almost completely abolished the pressor responses to stimulation of the entire sympathetic outflow in the pithed rat, the contractions of the lower eyelid to stimulation of the cervical sympathetic trunk and the vasconstrictor responses produced by periarterial nerve stimulation of the isolated renal artery preparation. Pressor responses to physostigmine and to tyramine were markedly reduced or abolished in anaesthetized and pithed rat preparations, respectively.
In corresponding experiments, 10‐week‐old rats treated as newborns with 6‐OHDA showed a marked reduction in the stimulation‐induced pressor responses and contractions of the lower eyelid, but completely normal vasoconstrictor responses to periarterial nerve stimulation of the isolated perfused renal artery were obtained. The pressor responses to physostigmine were slightly reduced but the tyramine responses were unchanged.
Treatment with 6‐OHDA at birth caused an almost complete and long‐lasting noradrenaline depletion in the heart, spleen, salivary glands and ileum but only a partial depletion in the mesentery from 10‐week‐old rats. These low noradrenaline levels showed no recovery in rats up to an age of 4 months. The tyrosine hydroxylase activity in both the cervical and stellate ganglia from 10‐week‐old rats was markedly reduced by treatment with 6‐OHDA after birth.
Injections of 6‐OHDA after birth produce an almost complete and permanent sympathectomy of various adrenergically innervated organs in the rat. The vascular system represents a major exception, exhibiting a surprisingly high resistance to this type of chemical adrenergic denervation.
Interaction of bretylium and guanethidine on the relaxations of the rat isolated fundal strip preparation, evoked by indirect stimulation
Authors: GAITONDÉ B. B. , NIMBKAR A. Y. 
Published: July 2012

Summary
Isolated rat stomach fundal strip bathed in Krebs solution containing atropine (1 μg/ml), responded to indirect stimulation by a relaxation which was frequency dependent. These responses were blocked by phenoxybenzamine (6 ftg/ml) or phentolamine (8 μg/ml).
Strips obtained from rats previously treated with reserpine did not show relaxation to indirect stimulation. These responses were therefore adrenergic in nature.
Bretylium (0·1–100 μg/ml) failed to block the relaxations produced by indirect stimulation, in fact relaxations were potentiated by the drug.
Guanethidine (10 μg/ml) blocked the relaxations induced by indirect stimulation.
Guanethidine may be taken up by adrenergic nerves actively since its action is not seen at 12° C.
Bretylium (10 μg/ml) prevented the actions of guanethidine at 37° C.
The release of spasmogenic substances from human chopped lung tissue and its inhibition
Authors: PIPER PRISCILLA J. , WALKER JOYCE L. 
Published: July 2012

Summary
Human lung tissue, passively sensitized with reaginic antibodies, released prostaglandins E1, E2 and F2α in addition to histamine and slow reacting substance (SRS‐A), when exposed to the appropriate antigen. No rabbit aorta contracting substance (RCS) was detected.
Experiments with rats and guinea‐pigs showed that the release of RCS is not confined to anaphylactic reactions mediated by non‐reaginic antibodies but may be a feature of anaphylaxis in guinea‐pigs alone.
Human lung tissue gently agitated with a blunt nylon rod liberated an E‐type prostaglandin and RCS in addition to histamine and SRS‐A.
Human isolated bronchial muscle was contracted by RCS.
Disodium cromoglycate antagonized the release of prostaglandins during anaphylaxis but not during agitation of human lung tissue, whereas indomethacin blocked the release of prostaglandins during agitation and anaphylaxis.
The release of an E‐type prostaglandin during anaphylaxis in human lung tissue, which inhibits the further release of histamine could be another example of the regulatory role of prostaglandins in body functions.
The removal of noradrenaline in the pulmonary circulation of rat isolated lungs
Authors: ALABASTER VALERIE A. , BAKHLE Y. S. 
Published: July 2012

Summary
Removal of noradrenaline by isolated lungs of the rat, perfused via the pulmonary artery with Krebs bicarbonate solution has been studied.
A constant removal (40·2%) was observed over a concentration range of 2–50 ng noradrenaline/ml (12–300 nM). At 100 ng/ml (600 nM), the removal is significantly reduced to 33·5%.
The removal of noradrenaline was inhibited by cocaine (1 μm), but not by normetanephrine (5 μm), metaraminol (10 μm), phenoxybenzamine (10 μm) and 5‐hydroxytryptamine (110 and 560 nM).
We conclude that the removal of noradrenaline in the lungs does not involve an uptake process comparable with those previously described for this amine. The uptake process for noradrenaline in the lung is similar to that for 5‐hydroxytryptamine and may be unique to this tissue.
The inhibitory effect of manganese on transmitter release at the neuromuscular junction of the toad
Authors: BALNAVE R. J. , GAGE P. W. 
Published: July 2012

Summary
Manganese, at low concentrations (0·5–2·0 mm), blocks neuromuscular transmission in toads. Endplate potentials (e.p.ps) are reduced in amplitude but the amplitude of miniature endplate potentials (m.e.p.ps) is, if anything, increased.
The release of transmitter by an action potential is reduced in solutions containing Mn, but is still well described by the Poisson equation.
Log‐log plots of e.p.p. quantal content (m) against [Ca] have a mean gradient of 3·73, and a model based on the co‐operative action of four calcium ions in excitation‐secretion coupling, and competitive inhibition by Mn, was constructed. The model, with its exponent of 4, is shown in fact to predict gradients of less than four for log‐log plots of m against [Ca].
The assumption of competitive inhibition by Mn was supported by modified Lineweaver‐Burk plots of m−¼ against 1 / [Ca]. The mean dissociation constants for Ca and Mn were 1·3 mm and 015 mm respectively. From the model, an upper estimate of the density of calcium* receptor sites' of 30 per square micron of nerve terminal was obtained.
In contrast to its inhibitory effect on evoked release, Mn increases the spontaneous release of transmitter. It is suggested that Mn may increase m.e.p.p. frequency by releasing Ca from an intracellular store.
Mechanism of potentiation by amines of non‐equilibrium blockade of the α‐adrenoceptor
Authors: KALSNER S. 
Published: July 2012

Summary
The mechanism by which sympathomimetic and certain other amines enhance blockade of the α‐adrenoceptors by the non‐equilibrium antagonist N‐ethoxycarbonyl‐2‐ethoxy‐1,2‐dihydroquinoline (EEDQ) in strips of rabbit aorta was examined.
Non‐equilibrium blockade of the 5‐hydroxytryptamine receptors by EEDQ was not increased by sympathomimetic amines and was decreased by 5‐hydroxytryptamine.
Low concentrations of reversible competitive antagonists appeared to protect selectively against the additional blockade by EEDQ which develops in the presence of an amine.
Phenoxybenzamine potentiated EEDQ blockade of the α‐receptors but not of the 5‐hydroxytryptamine receptors.
Augmentation of EEDQ blockade was also detected in a variety of other tissues, but not in segments of rabbit intestine where α‐adrenoceptors mediate an inhibitory response.
It was concluded that EEDQ acts at two sites in antagonizing α‐receptor mediated responses, and that one of these sites (site II) is separate from the site of action of agonists and phenoxybenzamine (site I). Amines which enhance blockade appear to exert their action by combining with a third site (site III), which may induce a conformational alteration at site II.
It appears that the α‐adrenoceptor may have multiple sites for drug interaction.
Effects of quazodine (MJ 1988) on contractions of the isolated hemidiaphragm of the rat and the biventer cervicis muscle of the chick
Authors: NOTT M. W. , WINSLOW EILEEN 
Published: July 2012

Summary
The effects of quazodine and theophylline have been studied on the rat hemidiaphragm and chick biventer cervicis preparations in vitro.
Theophylline and quazodine enhanced maximal twitches and contractural responses to acetylcholine and carbachol.
These actions on contractility were exerted directly upon the muscle fibres and were dependent upon the concentration of calcium ions in the bathing solution.
In addition, quazodine enhanced the neuromuscular blocking activity of tubocurarine, probably by a prejunctional action.
Theophylline potentiated acetylcholine to a greater extent than it potentiated carbachol thus suggesting that theophylline possesses anticholinesterase activity.
Response of the rat ileum, uterus and vas deferens to carbachol and acetylcholine following repeated daily administration of a cholinesterase inhibitor
Authors: FOLEY D. J. , McPHILLIPS J. J. 
Published: July 2012

Summary
Daily i.p. administration, for eight days, of the cholinesterase inhibitor disulfoton to rats produced mild to moderate signs of intoxication (tremors, incontinence and diarrhoea) but no deaths.
Segments of ileum taken from the treated rats were subsensitive to carbachol but the vas deferens and the uterus did not exhibit any change in sensitivity to carbachol.
The sensitivity to acetylcholine was increased in the ileum and vas deferens but not in the uterus.
Acetylcholinesterase activity was 60–70% inhibited in all three tissues.
Correlation between desipramine levels and (—)‐noradrenaline uptake and chronotropic effect in isolated atria of rats
Authors: BABULOVA A. , BAREGGI S. R. , BONACCORSI A. , GARATTINI S. , MORSELLI P. L. , PANTAROTTO C. 
Published: July 2012

Summary
The uptake of unlabelled and [14C]‐desipramine was studied in rat isolated atria incubated in a medium containing concentrations of desipramine ranging from 200 pg/ml to 2 μg/ml. The uptake was found to be dose‐ and time‐dependent. Equilibrium was not reached after 2–3 h of incubation unless concentrations of desipramine higher than 1 μg/ml were used.
The washout curves of atria previously loaded with desipramine showed that the drug is slowly released and that this release is not influenced by its initial tissue concentration.
The binding appeared to be at non‐specific sites and not at sites where noradrenaline is stored since atria taken from rats treated with 6‐hydroxydopamine accumulated the drug at the same rate as control atria.
The inhibition of (—)‐noradrenaline uptake and the potentiation of the chronotropic response to (—)‐noradrenaline is correlated with the concentration of desipramine in atria for tissue levels of the drug ranging from 001 to 1 μg/g. Higher tissue levels show less potentiation of the effect of (—)‐noradrenaline or even inhibition of the maximal response to (—)‐noradrenaline. These concentrations of desipramine (> 7 μg/g) markedly depressed the atrial rate.
The results show that despite the accumulation of desipramine by unspecific sites, concentrations of desipramine in the tissue are correlated with the pharmacological response. Furthermore a gradual shift from potentiation to inhibition of noradrenaline response can be obtained with the same bath concentrations of desipramine by increasing the time of incubation.
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 NaF
Authors: KATZ S. , TENENHOUSE A. 
Published: July 2012

Summary
A method for measuring the rate of production of 14C‐labelled adenine nucleotides, including cyclic adenosine 3′,5′monophosphate (cyclic AMP), from [14C]‐adenosinetriphosphate (ATP) was developed and used to study the effects of ATP, adenosine diphosphate (ADP) and adenosine 5′‐monophosphate (AMP) on the rate of accumulation of cyclic AMP in cell‐free preparations of adenyl cyclase from rat brain.
The mechanism by which NaF increases cyclic AMP accumulation was studied by comparing its effect on adenine nucleotide metabolism with that of an ATP regenerating system.
ADP and ATP are potent inhibitors of phosphodiesterase (PDE) and it is the sum of the concentrations of these two nucleotides which controlled the rate of destruction of cyclic AMP. The effect of these nucleotides was significant even in the presence of 6·7 mm theophylline; theophylline itself inhibited PDE only 50–60%.
Fluoride ion had no direct effect on PDE but it inhibited the rate of hydrolysis of ADP and ATP and thus indirectly inhibited PDE. The effect of fluoride ion on cyclic AMP accumulation can be explained, at least in part, by this indirect inhibition of PDE.
Studies on a more purified preparation of adenyl cyclase clearly demonstrated a direct action of NaF on adenyl cyclase.