bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE EFFECTS OF CYCLIC DICARBOXYLIC ACIDS ON SPONTANEOUS AND AMINO ACID‐EVOKED ACTIVITY OF RAT CORTICAL NEURONES
Authors: BIRLEY S. , COLLINS J.F. , PERKINS M.N. , STONE T.W. 
Published: July 2012

A series of cyclic dicarboxylic acids were applied by microiontophoresis to neurones in the cerebral cortex of rats anaesthetized with urethane. The object was to examine effects on spontaneous firing rates and any ability to antagonize responses to excitatory amino acids.
At relatively low ejecting currents (10–25 nA) cis‐2,3‐piperidine dicarboxylic acid (cis‐2,3‐PDA) had no effect on spontaneous firing but selectively antagonized the excitation evoked by N‐methyl‐D‐aspartate (NMDA) without affecting responses to quisqualate or kainate. At higher ejecting currents (60–100 nA) responses to all three agonists were reduced.
Other cis‐piperidine dicarboxylic acids and piperazine‐2, 3‐dicarboxylic acid had only weak and variable effects on cell firing and responses to NMDA, quisqualate, kainate, glutamate and aspartate.
2, 3‐Pyridine dicarboxylic acid (quinolinic acid) produced excitation of all cortical neurones tested.
2‐Amino‐5‐phosphono‐valeric acid, an NMDA antagonist, reduced responses to quinolinate, implying that this compound can act at NMDA receptors.
It is suggested that quinolinic acid may be of physiological interest as a potential endogenous excitant in the nervous system and that cis‐2,3‐PDA and its N‐methyl derivative may be of use in studies of receptor pharmacology and the identification of synaptic transmitters.
FIBRIN, RED CELL AND PLATELET INTERACTIONS IN AN EXPERIMENTAL MODEL OF THROMBOSIS
Authors: SMITH J.R. , WHITE A.M. 
Published: July 2012

Insertion of a cotton thread into an arteriovenous shunt of an anaesthetized rat causes an increase in the weight of the thread due to deposition of thrombus.
The thrombus formed was of the venous (red) type, being sensitive to heparin, yet possessed important characteristics of an arterial thrombus, in that it was dependent on platelets and on rate of blood flow.
Thromboxane synthetase inhibitors had no effect on thrombus deposition.
Cyclo‐oxygenase inhibitors did not significantly depress thrombus formation at doses which inhibited platelet function ex vivo.
Compounds which can modify the release or action of adenosine 5′‐diphosphate partly inhibited thrombus formation.
A depression in clotting factor levels induced by sodium warfarin led to a highly significant reduction in thrombus formation at doses which caused a prolongation of prothrombin clotting time.
ELECTRICAL SLOW WAVES AND TONE OF GUINEA‐PIG ISOLATED TRACHEALIS MUSCLE: EFFECTS OF DRUGS AND TEMPERATURE CHANGES
Authors: SMALL ROGER C. 
Published: July 2012

Simultaneous recordings of electrical and mechanical activity have been made from guinea‐pig isolated trachealis muscle. Electrical activity was recorded both by extracellular and intracellular techniques.
Extracellular studies showed that the spontaneous development of tone was accompanied by electrical slow waves which frequently exhibited pronounced waxing and waning. Intracellular recording confirmed the discharge of these slow waves in individual cells. Extracellularly‐recorded slow waves were often of greatest amplitude while the tissue was developing rather than maintaining tension. Some tissues became electrically quiescent on reaching peak tone.
Cooling to 27.5°C caused some relaxation. Slow wave amplitude and frequency fell, slow waves eventually being abolished. Subsequent rapid rewarming initially evoked a more profound relaxation. An intense discharge of slow waves then occurred as the tension rapidly rose again towards the pre‐cooling value.
Sodium nitrite, (−)‐isoprenaline, adenosine and adenosine triphosphate (ATP) each evoked relaxation and reduced the frequency and amplitude of slow waves. High concentrations of these agents often abolished slow waves. The actions of these drugs were reversible.
Treatment with methoxyverapamil (D600) 1 μmol/l for 15 min abolished slow wave activity but only evoked partial relaxation of the tissue.
Acetylcholine, histamine and tetraethylammonium (TEA) each evoked contraction, but TEA was unique in consistently promoting slow waves and (in high concentration) spike activity. Spasm evoked by acetylcholine and histamine did not usually involve the initiation or promotion of slow waves. Indeed in appropriate concentration these two agents always suppressed slow wave activity. The actions of the spasmogens were reversible.
It is concluded that the smooth muscle cells of the trachealis are electrically coupled. While co‐ordinated slow wave activity is associated with the spontaneous development of tension in trachealis, it may not be necessary for the maintenance of the major part of the spontaneous tension exhibited by the tissue or for the spasm evoked by histamine or acetylcholine. Slow wave promotion by TEA suggests that the tissue may have a high resting potassium conductance which normally attenuates the slow waves. Slow waves may be suppressed by a variety of drugs acting by different mechanisms. Since D600 suppresses slow waves of the trachealis the mechanisms underlying the waves may be similar to those underlying spike activity in other smooth muscles.
EFFECTS OF LYSINE‐VASOPRESSIN AND OXYTOCIN ON CENTRAL CARDIOVASCULAR CONTROL
Authors: TRAN LAC DANG , MONTASTRUC JEAN‐LOUIS , MONTASTRUC PAUL 
Published: July 2012

The cardiovascular effects of intravenous and intracisternal administration of neurohypophysial peptides were compared in dogs anaesthetized with chloralose.
Intravenous lysine‐vasopressin (0.1 to 100 mu/kg) induced a dose‐dependent increase in blood pressure and a decrease in heart rate. In contrast, intracisternal lysine‐vasopressin (0.01 to 10 mu/kg) induced a dose‐related decrease in blood pressure and did not change heart rate.
Intracisternal oxytocin (1 and 10 mu/kg) increased blood pressure and did not change heart rate, whereas the same doses injected intravenously were inactive.
Pretreatment with guanethidine (15 mg/kg i.v. 24 h beforehand) abolished the hypotensive responses to intracisternal vasopressin but not the pressor action of intravenous vasopressin.
The pressor responses to central injections of oxytocin were not modified by guanethidine.
Hypotension elicited by intracisternal vasopressin was probably due to a decrease in sympathetic tone whereas the hypertension induced by intracisternal oxytocin was independent of variations in sympathetic tone.
PRESYNAPTIC MUSCARINIC RECEPTORS INHIBITING ACTIVE ACETYLCHOLINE RELEASE IN THE BULLFROG SYMPATHETIC GANGLION
Authors: KOKETSU K. , YAMADA M. 
Published: July 2012

The effects of bethanechol and atropine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined electrophysiologically.
Bethanechol (1 mm) caused no depolarization of sympathetic preganglionic nerve terminals, whereas carbachol or ACh in the same concentration induced marked depolarizations of these terminals.
Bethanechol (10 μm) depressed the amplitude of fast excitatory postsynaptic potentials (e.p.s.ps) recorded in low Ca2+‐high Mg2+ solution, without depolarizing ganglion cells. The quantal content measured from these fast e.p.s.ps by the variance method showed a significant reduction.
Amplitudes of both miniature e.p.s.ps and ACh‐potentials induced by iontophoresis of ACh were not affected by addition of bethanechol (10 μm).
The depressant effect of bethanechol (10 μm) on fast e.p.s.ps disappeared in the presence of atropine (3 μm).
Atropine (3 μm) increased the quantal content measured from fast e.p.s.ps recorded in low Ca2+‐high Mg2+ solution.
The depressant effect of bethanechol (10 μm) on fast e.p.s.ps was unaffected by α‐adrenoceptor blocking agents (phenoxybenzamine (10 μm) or phentolamine (10 μm)).
These results suggest that presynaptic nerve terminals in bullfrog sympathetic ganglia possess a muscarinic receptor which inhibits active release of ACh.
THE EFFECTS OF VASOACTIVE INTESTINAL POLYPEPTIDE AND OF ADENOSINE 5′‐TRIPHOSPHATE ON THE ISOLATED ANOCOCCYGEUS MUSCLE OF THE MOUSE
Authors: GIBSON A. , TUCKER J.F. 
Published: July 2012

Vasoactive intestinal polypeptide (VIP, 0.01–5 μm) produced dose‐related relaxations of the mouse anococcygeus muscle.
Following incubation with indomethacin (2.8 μm 1 h) adenosine 5′‐triphosphate (ATP, 0.5–10 mm) produced dose‐related relaxations of the mouse anococcygeus.
Haemolysed blood reduced inhibitory responses of the mouse anococcygeus to field stimulation but had no effect on relaxations to VIP or ATP.
Apamin (0.5 μm) had no effect on the relaxation of mouse anococcygeus to field stimulation, VIP, or ATP.
2‐2′‐Pyridylisatogen tosylate (PIT, 50 μm) itself reduced muscle tone but it did not abolish inhibitory responses to field stimulation, VIP, or ATP.
During prolonged inhibitory nerve stimulation the relaxation of the mouse anococcygeus in response to VIP was reduced greatly while that to ATP was unaffected.
Bundles of VIP‐immunoreactive sites were detected in sections of the mouse anococcygeus treated by the peroxidase‐antiperoxidase (PAP) immunocytochemical technique.
The results suggest that the mechanisms underlying non‐adrenergic, non‐cholinergic inhibitory transmission in the mouse anococcygeus are similar to those in the bovine retractor penis and unlike those in the guinea‐pig taenia caeci.
The possibility that VIP or ATP might be involved in inhibitory neurotransmission in the mouse anococcygeus is discussed.
A STUDY OF α1‐ADRENOCEPTORS IN RAT RENAL CORTEX: COMPARISON OF [3H]‐PRAZOSIN BINDING WITH THE α1‐ADRENOCEPTOR MODULATING GLUCONEOGENESIS UNDER PHYSIOLOGICAL CONDITIONS
Authors: McPHERSON G.A. , SUMMERS R.J. 
Published: July 2012

A comparison has been made of the α1‐adrenoceptor controlling gluconeogenesis in tubules from rat renal cortex and [3H]‐prazosin binding in membranes prepared from the same tissue under physiological conditions.
In renal tubules the α‐adrenoceptor agonists, oxymetazoline, (−)‐noradrenaline, (−)‐α‐methylnoradrenaline and (−)‐phenylephrine, stimulated gluconeogenesis from pyruvate. Oxymetazoline was the most potent agonist (EC50 15.7 nm) but produced only 61% of the maximum response elicited by (−)‐noradrenaline.
The α‐adrenoceptor antagonists, BE2254, prazosin, indoramin and phentolamine inhibited (−)‐noradrenaline‐mediated increases in gluconeogenesis. The α1‐adrenoceptor selective compounds, BE2254 and prazosin, were the most effective antagonists with KB values of 0.74 and 1.47 nm respectively.
[3H]‐prazosin binding to membranes prepared from rat renal cortex in physiological saline at 37°C was best described by a two site model. High affinity, but not low affinity sites had characteristics consistent with α‐adrenoceptors.
High affinity [3H]‐prazosin binding could be completely displaced by the α‐adrenoceptor agonists, oxymetazoline, (−)‐noradrenaline, (−)‐phenylephrine, and (−)‐α‐methylnoradrenaline. Slope factors for the displacement curves were all significantly less than unity. The concentrations of agonists required to displace [3H]‐prazosin binding were markedly higher than those required to stimulate gluconeogenesis.
High‐affinity [3H]‐prazosin binding was also displaced by the α‐adrenoceptor antagonists, prazosin, BE2254, phentolamine and indoramin. Slope factors for the displacement curves were close to unity. Ki values calculated from the binding experiments were very similar to KB values obtained in the gluconeogenesis studies. These results suggest that in rat renal cortex the α1‐adrenoceptor labelled by [3H]‐prazosin is probably that which stimulates gluconeogenesis.
The biological activity of a single dose of tamoxifen in the adult ovariectomized rat
Authors: Bowman Susan P. , Jones Christine A. , Leake A. , Morris I.D. 
Published: July 2012

The peripheral and central activities of tamoxifen were studied in the ovariectomized adult rat, up to 16 d after a single dose of 7.0 or 0.7 mg/kg.
Food consumption and body weight were decreased; only food consumption returned to control values after 16 d.
The weights of the uterus and of the uterine luminal fluid were increased for up to 8 d.
Serum follicle‐stimulating hormone (FSH) concentrations decreased, but only significantly 1 and 8 d after 7.0 mg tamoxifen/kg. Serum luteinizing hormone (LH) and prolactin concentrations were elevated for up to 4 d.
Lordosis behaviour was absent throughout the period studied.
Within 3 d of administration, tamoxifen partially antagonized the oestrogen‐induced changes in uterine luminal fluid, prolactin and LH secretion and lordosis behaviour.
Tamoxifen did not alter oestrogen‐induced changes in uterine weight, food consumption and body weight.
The experiments demonstrate that tamoxifen is active for up to 16 d after a single intraperitoneal dose; oestrogen agonist, partial agonist and antagonist activities were demonstrated. The duration and type of activity depends upon the dose of tamoxifen and the target tissue response examined.
The role of nicotinic receptors in dog pancreatic exocrine secretion
Authors: Devaux M.A. , Diaz G.R. , Kubota K. , Magee D.F. , Sarles H. 
Published: July 2012

The effects of pentamethonium, an autonomic ganglion blocker, were studied on the exocrine pancreatic secretion of six conscious dogs given intravenous infusions of urecholine, caerulein or pentagastrin on a background of submaximal doses of secretin.
Urecholine‐induced protein secretion was not affected but both caerulein‐ and to a smaller extent, pentagastrin‐induced protein secretions were depressed by pentamethonium.
These results indicate that intravenous caerulein and pentagastrin, but not urecholine, act at least partially via nicotinic receptors.
Volume and bicarbonate output were depressed by pentamethonium when stimulated by intravenous caerulein with a background of secretin, but not when stimulated by pentagastrin on a background of secretin.
From these data it is suggested that caerulein and pentagastrin may potentiate secretin‐stimulated hydrelatic secretion by different mechanisms.
Release of [3H]‐amezinium from cortical noradrenergic axons: a model for the study of the α‐autoreceptor hypothesis
Authors: Hedler Liselotte , Starke Klaus , Steppeler Anton 
Published: July 2012

[3H]‐amezinium is taken up selectively into noradrenergic axons and their transmitter‐storing vesicles and is released from these axons by action potentials. We used it as a non‐α‐adrenergic marker in order to study the α‐adrenergic autoinhibition of noradrenaline release.
Rat occipitocortical slices were preincubated with [3H]‐amezinium 0.03 μm and then superfused and stimulated electrically (3 Hz for 3 min). The stimulation‐evoked overflow of tritium was measured in six groups of slices: from saline‐pretreated rats; from saline‐pretreated rats, the slices being exposed to exogenous noradrenaline before preincubation with [3H]‐amezinium; from saline‐treated rats, slices from which were exposed simultaneously to noradrenaline and cocaine before preincubation with [3H]‐amezinium; from rats in which noradrenaline stores had been depleted by pretreatment with α‐methyltyrosine (α‐MT); from α‐MT‐treated rats, the slices being exposed to noradrenaline before preincubation with [3H]‐amezinium; and from α‐MT‐treated rats, slices from which were exposed to noradrenaline plus cocaine before preincubation with [3H]‐amezinium.
The stimulation‐evoked overflow of tritium, expressed as a percentage of the tritium content of the tissue, was 1.15% in slices from saline‐pretreated rats, and was similar in slices from saline‐pretreated rats after exposure to noradrenaline or noradrenaline plus cocaine. It was 2.56% in slices from α‐MT‐treated rats, 1.20% from α‐MT‐treated rats after exposure to noradrenaline, and 2.88% from α‐MT‐treated rats after exposure to noradrenaline plus cocaine.
Yohimbine 0.1 and 1 μm increased the stimulation‐evoked overflow of tritium in slices from all groups of saline‐pretreated rats and in those slices from α‐MT rats that had been in contact with exogenous noradrenaline. Yohimbine did not change the evoked overflow in slices from α‐MT rats that had not been exposed to noradrenaline, or had been exposed to noradrenaline plus cocaine.
Clonidine 0.01 — 1 μm decreased the stimulation‐evoked overflow of tritium moderately in slices from saline‐pretreated rats, markedly in slices from α‐MT‐treated rats, and moderately again when the latter slices had been exposed to noradrenaline.
It is concluded that the action potential‐evoked release of [3H]‐amezinium as well as the modulation of this release by yohimbine and clonidine depend on the presence or absence of α‐adrenergic autoinhibition caused by the co‐secretion of noradrenaline. When there is co‐secretion of noradrenaline, the evoked release of [3H]‐amezinium is relatively small, yohimbine increases the release, and clonidine can cause only moderate inhibition. When there is no or very little co‐secretion of noradrenaline, the evoked release of [3H]‐amezinium is at least doubled, yohimbine causes no further increase and clonidine produces strong inhibition.
An investigation of presynaptic α‐adrenoceptor subtypes in the pithed rat heart
Authors: Docherty James R. 
Published: July 2012

The presynaptic cardio‐inhibitory and postsynaptic pressor responses to the α‐adrenoceptor agonists xylazine and cirazoline, and the interaction with the antagonists yohimbine and prazosin, were examined in the pithed rat.
Evidence was found to suggest that, as well as the already established pre‐ and postsynaptic α2‐and postsynaptic α1‐receptors, presynaptic α1‐receptors are present.
Topical capsaicin pretreatment inhibits axon reflex vasodilatation caused by somatostatin and vasoactive intestinal polypeptide in human skin
Authors: Anand P. , Bloom S.R. , McGregor G.P. 
Published: July 2012

Wheal and flare reactions are described following intradermal injections of somatostatin, vasoactive intestinal polypeptide, substance P and histamine in normal human forearm skin. Bombesin failed to produce a significant wheal and flare.
Pretreatment of skin with capsaicin in all cases dramatically inhibited the flare but not the wheal. This result is in accord with the hypothesis that capsaicin blocks the effector side of the axon reflex, perhaps by depleting nerve terminals of vasodilatory peptide(s).
Aortic vascular and atrial responses to (±)‐1‐O‐octadecyl‐2‐acetyl‐glyceryl‐3‐phosphorylcholine
Authors: Cervoni P. , Herzlinger H.E. , Lai F.M. , Tanikella T.K. 
Published: July 2012

The effects of (±)‐1‐O‐octadecyl‐2‐acetyl‐glyceryl‐3‐phosphorylcholine (octadecyl‐AGPC) were studied in three types of aortic vascular smooth muscle preparations, namely, strips, rubbed and unrubbed rings, and an atrial preparation in normotensive rats.
In the resting tension state, octadecyl‐AGPC did not elicit significant contractions in either rubbed or unrubbed ring preparations at concentrations lower than 1 × 10−4m. However, at a concentration of 3 × 10−4 m, octadecyl‐AGPC markedly contracted both types of ring preparations. This contractile response was partially antagonized by pretreatment with reserpine and completely blocked by phentolamine (1 × 10−6m).
In preparations contracted with noradrenaline (NA), octadecyl‐AGPC elicited biphasic responses in intact ring preparations; an initial relaxation followed by contraction. Octadecyl‐AGPC induced only a slight contraction in strips and a slight relaxation in the rubbed ring preparation.
Octadecyl‐AGPC did not elicit any significant effect on chronotropy or inotropy at concentrations up to 3 × 10−5 m. When the concentration was 1 × 10−4 m, octadecyl‐AGPC produced significant positive chronotropic and inotropic effects on spontaneously beating right and electrically driven left atrial preparations, respectively. Both effects were blocked by propranolol (5 × 10−8m); reserpine pretreatment antagonized only the chronotropic response.
In [3H]‐dihydroalprenolol ([3H]‐DHA) binding studies, octadecyl‐AGPC had a Kd of 427.85 μm and thus was much less potent than isoprenaline (Kd = 465.10 nm) or propranolol (Kd = 4.4 nm) in displacing [3H]‐DHA in rat cardiac membrane preparations.
In conclusion, relaxation and contraction induced by octadecyl‐AGPC in aortic preparations is an indirect rather than a direct effect. An unknown factor released from endothelial cells is responsible for aortic smooth muscle relaxation by octadecyl‐AGPC while released NA appears to be responsible for aortic vascular contraction and for the positive chronotropic and inotropic effects in the atrial preparations.
Platelet β‐adrenoceptors
Authors: Kerry Roger , Scrutton Michael C. 
Published: July 2012

Inhibition by isoprenaline of the aggregatory response of human and rat platelets induced by various excitatory agonists is blocked by β2‐adrenoceptor antagonists, β1‐Adrenoceptor antagonists are ineffective.
β2‐Adrenoceptor agonists cause inhibition of the response of human platelets to various excitatory agonists. The maximal extent of inhibition is less than that observed for isoprenaline. β1‐Adrenoceptor agonists fail to cause detectable inhibition of this response. Neither β1 nor β2‐adrenoceptor agonists cause inhibition of the response of rat platelets to excitatory agonists. Only β2‐adrenoceptor agonists block the inhibitory response to isoprenaline.
The extent of inhibition by isoprenaline is a function of the excitatory agonist used and in human platelets is correlated with the ability of that agonist to suppress elevated platelet cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) levels.
Inhibition by isoprenaline is prevented in the presence of an inhibitor of adenylate cyclase.
Isoprenaline increases platelet cyclic AMP levels with an EC50 similar to that required to observe inhibition of the aggregatory response.
These data indicate that human platelets carry β2‐adrenoceptors whose occupancy causes inhibition of the response to excitatory agonists as a consequence of elevation of platelet cyclic AMP. The β‐adrenoceptor present on rat platelets also appears to be of the β2‐subtype.
Cardiovascular responses of rats to intrahypothalamic injection of carbachol and noradrenaline
Authors: Poole S. 
Published: July 2012

Carbachol (0.1–2 μg) and noradrenaline (5–20 μg) injected into the anterior hypothalamus of unanaesthetized unrestrained rats evoked dose‐dependent falls in heart rate and increases in arterial blood pressure.
When the above amine injections were repeated in rats anaesthetized with chloral hydrate, sodium pentobarbitone or halothane the evoked bradycardias were usually smaller and the changes in arterial blood pressure more variable.
The cardiovascular responses to carbachol (1 μg) and to noradrenaline (10 μg) were antagonized by intrahypothalamic injection of atropine (1 μg) and phentolamine (10 μg), respectively.
The bradycardias evoked by carbachol (1 μg) and by noradrenaline (10 μg) were abolished by pretreatment with intra‐arterial injection of methyl atropine (100 μg 100 g−1).
The hypertensive responses to carbachol (1 μg) and to noradrenaline (10 μg) were reduced by pretreatment with intra‐arterial injection of thymoxamine (500 μg 100 g−1).