bluuebunny/crossref_metadata_2025_split huggingface dataset:
CENTRAL MECHANISM OF VASOPRESSIN‐INDUCED CHANGES IN ANTIDIURETIC HORMONE RELEASE
Authors: BHARGAVA K.P. , KULSHRESTHA V.K. , SRIVASTAVA Y.P. 
Published: July 2012

Intracerebroventricularly (i.c.v.) administered vasopressin (0.001–1.0 u) in dogs anaesthetized with chloralose produced a dose‐dependent increase in urine flow with a concomitant decrease in the levels of antidiuretic hormone (ADH) in jugular vein blood.
Higher doses of vasopressin (1.5–2.0 u, i.c.v.) on the other hand had an antidiuretic effect and produced an increase in blood ADH level.
Pretreatment (i.c.v.) with a β‐adrenoceptor antagonist completely blocked the diuretic response of low doses of vasopressin (i.c.v.) but did not influence the antidiuretic response obtained with high doses.
Repeated administration of vasopressin (1.0 u, i.c.v.) induced tachyphylaxis; central catecholamine depletion with tetrabenazine significantly inhibited the vasopressin‐induced diuretic response.
It is concluded that intracerebroventricular vasopressin‐induced changes in ADH secretion are mediated through the release of catecholamines in the central nervous system.
PRENYLAMINE‐INDUCED CONTRACTURE OF FROG SKELETAL MUSCLE
Authors: KIRSTEN E.B. , LUSTIG KAREN C. 
Published: July 2012

Experiments were performed to determine the influence of prenylamine on excitation‐contraction coupling in frog sartorius muscle.
Prenylamine (0.2‐1.0 mM) produced a biphasic contracture in skeletal muscle characterized by an initial phasic and subsequent tonic contracture.
Neither dantrolene nor procaine blocked the prenylamine‐induced contracture. Pretreatment with 100 mM K+ blocked the phasic but not the tonic component of the prenylamine contracture.
Prenylamine produced a sustained increase in 45Ca efflux at all concentrations that produce contracture. These concentrations of prenylamine also depressed the action potential, muscle twitch and resting potential.
Low concentrations of prenylamine (0.05 mM) which produced neither contracture, 45Ca efflux nor 45Ca influx, depressed the action potential, muscle twitch and K+ contracture.
The results suggest that prenylamine not only alters calcium mobility but also membrane permeability to other ions.
SELECTIVE INHIBITORY ACTIONS OF SODIUM‐p‐BENZYL‐4‐[1‐OXO‐2‐(4‐CHLOROBENZYL)‐3‐PHENYL PROPYL] PHENYL PHOSPHONATE (N‐O164) AND INDOMETHACIN ON THE BIOSYNTHESIS OF PROSTAGLANDINS AND THROMBOXANES FROM ARACHIDONIC ACID
Authors: EAKINS K.E. , KULKARNI P.S. 
Published: July 2012

Sodium p‐benzyl‐4‐[1‐oxo‐2‐(4‐chlorobenzyl)‐3‐phenyl propyl]phenyl phosphonate (N‐0164) selectively inhibited the formation of thromboxane‐A2 from prostaglandin endoperoxides by human platelet microsomes in a dose‐dependent manner (IC50 2.2 × 10−5 m or 11.6 μg/ml).
N‐0164 was approximately 15 to 20 times as potent as indomethacin as an inhibitor of thromboxane‐A2 formation. In contrast, indomethacin was 20 times as potent as N‐0164 as an inhibitor of prostaglandin endoperoxide formation from arachidonic acid (IC50 2.6 × 10−5 m or 9.4 μg/ml).
Spiral strips of dog coronary arteries relaxed in the presence of prostaglandin endoperoxides and were contracted by prostaglandin E2 and thromboxane‐A2 and were therefore used to distinguish between prostaglandins and their intermediate precursors, the endoperoxides.
Neither indomethacin nor N‐0164 (both 50 μg/ml) significantly inhibited the formation of prostaglandin‐like activity from the endoperoxides following incubation with indomethacin‐pretreated rabbit kidney medulla microsomes.
It is not known whether this action of N‐0164 is related to its ability to antagonize certain actions of prostaglandins (and related compounds) or whether N‐0164 can penetrate the cell membrane to inhibit thromboxane formation in the intact cell.
Selective inhibition of thromboxane formation by drugs such as N‐0164 may be useful both clinically and as a pharmacological tool to elucidate the patho‐physiological roles of the thromboxanes.
THE EFFECTS OF GASTRIN AND GASTRIN ANALOGUES ON PANCREATIC ACINAR CELL MEMBRANE POTENTIAL AND RESISTANCE
Authors: IWATSUKI N. , KATO K. , NISHIYAMA A. 
Published: July 2012

Intracellular recordings of membrane potentials and input resistance have been made from the exocrine acinar cells of mouse and rat pancreas placed in a tissue bath perfused with Krebs‐Henseleit solution.
The resting acinar cell membrane potential was about −38 mV. The acinar cells were stimulated by cholecystokinin‐pancreozymin (CCK‐PZ), gastrin and the gastrin‐related polypeptides, caerulein and desulphated caerulein. The immediate effect of stimulation with these secretagogues was always a depolarization and a concomitant reduction in input resistance and time constant. Depolarization of the acinar cell membrane by these secretagogues was not abolished in the presence of atropine (1.4 μm).
These peptide secretagogues were divided into the gastrin group and the CCK‐PZ group according to the time course of the depolarizations and the shape of the dose‐response curve. The depolarization evoked by the gastrin group returned quickly to the resting level but that evoked by the CCK‐PZ group was long lasting. The time course and the dose‐response curve for desulphated caerulein was identical with that of gastrin.
It was confirmed electrophysiologically that the activity of gastrin is exerted by the C‐terminal tetrapeptide; but the activity of caerulein depends on the C‐terminal heptapeptide, especially the presence in the molecule of the sulphated tyrosyl residue at position 7 (numbering from the C‐terminus). The equivalent sulphated tyrosyl residue in CCK‐PZ is probably necessary for optimal activity of this polypeptide.
The dose‐response curves obtained by electrophysiological methods indicated that the relative potencies of the peptides on mouse pancreatic acinar cells were caerulein > CCK‐PZ > gastrin. Synthetic human gastrin I was found to have a higher potency than either tetra‐ or pentagastrin.
A STUDY OF THE INTERACTIONS BETWEEN GLUTAMATE AND ASPARTATE AT THE LOBSTER NEUROMUSCULAR JUNCTION
Authors: NISTRI A. , CONSTANI A. 
Published: July 2012

The depolarizations produced by bath‐applied or iontophoretically applied glutamate and aspartate were recorded from lobster muscle fibres by means of intracellular microelectrodes.
Bath‐applied glutamate or aspartate evoked reversible, membrane depolarizations; however, responses to repeated applications of aspartate decreased progressively in amplitude until a plateau level was attained. Repeated applications of glutamate, kainate, domoate or quisqualate did not produce a similar effect.
After a dose of glutamate, responses to bath‐applied aspartate were enhanced. Responses to other depolarizing agonists were little affected by previous administration of glutamate. Aspartate dose‐depolarization curves were therefore constructed after initial aspartate responses had stabilized. The log‐log transforms of the aspartate and glutamate curves had limiting slopes of 0.8 and 2.1 respectively.
Iontophoretic application of aspartate to single glutamate‐sensitive sites produced small depolarizations with slow time course, compared with the glutamate potentials. When aspartate and glutamate were pulsed simultaneously from a twin‐barrelled pipette, the resultant glutamate potential was enhanced. It is suggested that this potentiation was due to summation of agonist concentrations in the receptor region interacting with a second‐order dose‐response relationship.
Bath‐applied aspartate increased the amplitude and prolonged the half‐decay time of the glutamate potential. This effect was particularly noticeable when the glutamate potential was of slow time course.
It is proposed that bath‐applied aspartate has an agonist effect whose magnitude is possibly exaggerated by concomitant release of glutamate and/or inhibition by glutamate of aspartate uptake. This agonist action of aspartate is thought to be exerted mainly on extrajunctional areas of the glutamate‐sensitive sites.
THE ACUTE EFFECTS OF NICOTINE, TOBACCO SMOKE AND CARBON MONOXIDE ON MYOCARDIAL OXYGEN TENSION IN THE ANAESTHETIZED CAT
Authors: RINK RICHARD D. 
Published: July 2012

The acute effects of nicotine, tobacco smoke, and carbon monoxide on myocardial oxygen tension (MPo2) were estimated amperometrically in 33 anaesthetized open‐chest cats with a glass‐insulated 25 gtm platinum cathode within a 22‐gauge needle implanted in the left ventricular wall.
MPo2 was 1.6–60 mmHg (mean 23.5 mmHg) when arterial P02 was >80 mmHg. Sequential intravenous infusions of nicotine (2–3 gg/kg every 45 s) or intracheal puffs (3–5 ml) of tobacco smoke commonly produced transitory increases (25–35 mmHg) of arterial pressure and 4–6 mmHg increments of MPo2. Intratracheal puffs (5 ml) of 5% carbon monoxide sufficient to increase carboxyhaemoglobin from 0.8 to 1.5% to 4–7% had no effect on arterial Po2 or blood pressure but typically decreased MPo2 by approximately 1–4 mmHg. Augmentation of MPo2 often succeeded carbon monoxide administration.
Arterial hypoxia (arterial Po2 < 60 mmHg) reduced mean MPo2 to 14.4 mmHg but anoxic levels were not observed. Pressor responses to nicotine and tobacco smoke were accompanied by small increases (usually 1–3 mmHg) of MPo2. Puffs of 5% carbon monoxide had less effect than during normoxia. Locations of low MPo2 (<10 mmHg) were unaffected as carboxyhaemoglobin was raised to 7–11% during hypoxaemia.
It is concluded that nicotine and tobacco smoke cause augmentation of myocardial oxygen supply, even during moderate hypoxaemia. By contrast, smoking dosages of carbon monoxide have the potential of producing a small reduction of MPo2 during normoxia, but the effect is negligible during moderate hypoxaemia.
ACTION OF GUANETHIDINE ON RABBIT ATRIAL MEMBRANES
Authors: MISU Y. , NISHIO H. 
Published: July 2012

Intracellular potentials were recorded in driven left atria from reserpine‐treated rabbits. Guanethidine 2 × 10−5m slightly increased Vmax and shortened the total duration (TD) of the action potential (AP) without causing hyperpolarization. For the first 30 min after 4 × 10−4m, Vmax increased without hyperpolarization and AP height increased slightly. Thereafter, Vmax and height decreased with a slight and gradual depolarization. This depolarization was irreversible. TD was increased after 15 minutes. Guanethidine 2 × 10−3 M initially decreased Vmax and height before causing depolarization.
Pretreatment with tetrodotoxin (TTX) 1.6 × 10−7m prevented or reversed the initial increases in Vmax, height and TD induced by guanethidine (4 × 10 −4m).
TTX 3.1 to 6.2 × 10−6m, added 15 or 30 min after guanethidine 4 × 10−4m, delayed or prevented depolarization by guanethidine.
Ouabain 10−5m incubated for 20 and 90 min greatly inhibited Na+, K+‐adenosine triphosphatase and K+‐phosphatase activities; guanethidine was without effect.
Guanethidine probably increases resting sodium permeability after the promotion of increases in sodium permeability during the AP. High doses of the drug decrease sodium permeability during the AP.
THE EFFECT OF DIPHENIDOL ON OUABAIN CARDIOTOXICITY IN THE CAT
Authors: BOUNOUS H. , CAGIN N. , LEVITT B. , SOMBERG J. 
Published: July 2012

The capacity of diphenidol to influence ouabain‐induced cardiotoxicity was studied in anaesthetized cats with and without spinal cord transection.
Diphenidol pretreatment increased the lethal dose of ouabain in both intact cats and cats in which the spinal cords had been transected. Diphenidol pretreatment increased the myocardial content of ouabain associated with death in the intact animals, but failed to influence the lethal ventricular concentration in cats with transected spinal cords.
The failure of diphenidol to influence tissue thresholds for toxicity in the spinal cat and the equivalence of tissue ouabain requirements for death in spinal cats and diphenidol‐treated intact animals, suggest a neural mechanism for the protective effect in intact animals.
Ouabain administration prolonged atrio‐ventricular conduction time in all animals and diphenidol attenuated this effect. Thus, the influence of both drugs on atrioventricular conduction may not be entirely mediated by central neurones.
STIMULATION OF PRESYNAPTIC β‐ADRENOCEPTORS ENHANCES [3H]‐N0RADRENALINE RELEASE DURING NERVE STIMULATION IN THE PERFUSED CAT SPLEEN
Authors: CELUCH STELLA M. , DUBOCOVICH MARGARITA L. , LANGER S.Z. 
Published: July 2012

The effects of isoprenaline, propranolol and phosphodiesterase inhibitors on 3H‐transmitter overflow elicited by low frequency nerve stimulation were determined in the isolated perfused spleen of the cat.
(‐)‐Isoprenaline (0.14, 1.4, and 14 nm) produced a concentration‐dependent increase in [3H]‐transmitter overflow evoked by nerve stimulation at 1 Hz and was more effective at 1 Hz than at 2 hertz.
A concentration of propranolol (0.1 μm), devoid of neurone blocking activity, blocked this effect of (—)‐isoprenaline. These results are compatible with the presence of β‐adrenoceptors in the noradrenergic nerve endings of the cat spleen.
(‐l‐)‐Isoprenaline (140 nm) failed to increase the release of radioactivity induced by nerve stimulation, indicating that the β‐adrenoceptor mediating the facilitation of transmitter release was stereo‐specific.
The increase in 3H‐transmitter overflow induced by nerve stimulation during exposure to the phosphodiesterase inhibitor, papaverine (27 μm) was more pronounced than that obtained in the presence of 3‐isobutyl‐l‐methyl xanthine (IBMX) 0.5 mm. The facilitation in transmitter release induced by papaverine was not correlated with the granular effect produced by this drug.
In the presence of papaverine, the concentration‐effect curve for (—)‐isoprenaline on transmitter release was shifted to the left and its maximum was increased. In addition, propranolol significantly reduced the enhancement in noradrenaline release obtained by exposure to papaverine under conditions in which the granular effect produced by the phosphodiesterase inhibitor was even greater than in the absence of the P‐blocker.
It is concluded that activation of presynaptic p‐adrenoceptors in the perfused cat spleen leads to an enhancement in transmitter release which appears to be linked to an increase in cyclic adenosine 3′, 5′‐monophosphate levels in noradrenergic nerve endings.
THE EFFECTS OF d‐PENICILLAMINE AND LEVAMISOLE ON LEUCOCYTE CHEMOTAXIS IN THE RAT
Authors: CUNNINGHAM F.M. , FORD‐HUTCHINSON A.W. , OLIVER A.M. , SMITH M.J.H. , WALKER J.R. 
Published: July 2012

The administration of D‐penicillamine (25 mg/kg) or levamisole (5 mg/kg) had no effect on leucocyte emigration into the exudates formed in inert sponges implanted in normal rats.
In rats, previously sensitized to Bordetella pertussis and implanted with sponges containing pertussis vaccine, an increased leucocyte migration into the exudates occurred; this was significantly enhanced by the administration of the drugs.
Neither drug in vitro affected the chemotaxis of rat polymorphonuclear leucocytes although random migration was significantly increased by levamisole (2 μg to 1 mg/ml). Neither drug affected the chemotaxis of rat mononuclear cells although levamisole (25 μg/ml) significantly increased that of human monocytes.
It is concluded that both drugs produce similar effects in an animal model of delayed hypersensitivity and that their clinical antirheumatic actions may have common elements.
THE EFFECTS OF AMINO ACIDS AND ANTAGONISTS ON THE ISOLATED HEMISECTED SPINAL CORD OF THE IMMATURE RAT
Authors: EVANS R.H. 
Published: July 2012

Records of ventral and dorsal root polarity of the isolated hemisected spinal cord of the 3‐9 day old rat showed that respective dose‐dependent depolarizations of motoneurones (VR responses) and primary afferent terminals (DR responses) were produced by both acidic and neutral amino acids in the presence of procaine (1 mM) or tetrodotoxin (0.1 μM).
Of the four neutral amino acids, γ‐aminobutyrate (GABA), glycine, taurine, and β‐alanine, GABA was the most effective in producing DR responses and glycine the most effective in producing VR responses. Only taurine depressed the electrical activity recorded from ventral roots.
The DR responses produced by GABA, β‐alanine and taurine, were all antagonized by bicuculline (5 μM) and picrotoxin (5 μM). Bicuculline was more selective than picrotoxin in antagonizing VR responses produced by GABA.
Strychnine (1 μM) antagonized VR responses produced by glycine β‐alanine and taurine without affecting responses produced by GABA. DR responses to the neutral amino acids were unaffected by strychnine.
ENHANCEMENT BY OXOTREMORINE OF ACETYLCHOLINE RELEASE FROM THE RAT PHRENIC NERVE
Authors: DAS M. , GANGULY D.K. , VEDASIROMONI J.R. 
Published: July 2012

Oxotremorine (10.5 μM) produced a paralytic effect on twitch responses of rat diaphragm in vitro to direct and indirect stimulation.
The paralytic effect of oxotremorine was absent when the diaphragm was stimulated directly in the presence of hemicholinium‐3 (0.42 mM), at a time when twitch responses to indirect stimulation ceased completely.
Oxotremorine, at two different pharmacologically active doses, strikingly increased the resting as well as electrically evoked release of acetylcholine into the bathing fluid from the phrenic nerve‐diaphragm preparation.
This presynaptic effect of oxotremorine may explain its pharmacological effects at the cholinergic synapses studied so far.
RELEASE OF NORADRENALINE FROM CAT SPLEEN SLICES BY POTASSIUM
Authors: GARCÍA A.G. , KIRPEKAR S.M. , PASCUAL R. 
Published: July 2012

When cat spleen slices were exposed to a potassium‐enriched (140mM) Krebs solution, 367 ± 31 ng g−1 5 min−1 of noradrenaline (NA) was released into the bathing medium.
Phenylephrine and clonidine (10−7 to 10−3M) did not significantly modify the potassium‐evoked NA release; acetylcholine decreased it in a dose‐dependent manner.
Phenoxybenzamine increased NA release by 50% but phentolamine did not alter it; high concentrations of this drug greatly decreased NA release. Cocaine increased the NA release by about 30%.
It is suggested that the failure of sympathomimetic amines to depress, and of α‐adrenoceptor blocking agents to enhance the release of NA by high potassium concentrations may be related to prolonged depolarization of the nerve terminals, which may desensitize presynaptic α‐receptors. The fact that the same drugs are able to modify NA release during electrical nerve stimulation may be ascribed to the much shorter periods of depolarization occurring under these conditions.
SODIUM‐DEPENDENT CARDIAC GLYCOSIDE BINDING: EXPERIMENTAL EVIDENCE AND HYPOTHESIS
Authors: FRICKE U. , KLAUS W. 
Published: July 2012

The influence of increasing Na+ concentrations on the binding of digitoxin, digoxin and ouabain was examined in a Na+‐K+‐ATPase preparation of guinea‐pig hearts
Two distinct processes seem to be involved in this interaction: one binding process was activated at low Na+ concentrations. The maximum binding capacities were different and the K0.5 values were nearly identical for the cardiac glycosides studied.
In contrast, the second binding process was activated at appreciably higher Na+ concentrations, the maximum binding capacities were almost identical and the K0.5 values were different for the cardiac glycosides studied.
On the basis of these results attempts are made to explain the well known differences in the myocardial accumulation of cardiac glycosides.
EFFECTS OF END‐TIDAL CONCENTRATIONS OF CYCLOPROPANE, HALOTHANE AND DIETHYL ETHER ON PERIPHERAL AUTONOMIC NEUROEFFECTOR SYSTEMS IN THE RAT
Authors: CLANACHAN A.S. , MUIR T.C. 
Published: July 2012

The effects of the inhalation anaesthetics, cyclopropane, halothane and diethyl ether were examined on peripheral neuroeffector systems in the pithed and in the conscious rat.
In the absence of a suitable means of accurately quantifying doses of inhalation anaesthetics given to small animals, an apparatus was constructed whereby end‐tidal gas samples were collected semi‐automatically from the mechanically ventilated rat.
Cyclopropane (15.3 and 29.3% end‐tidal), halothane (0.20, 0.52 and 0.83% end‐tidal) and diethyl ether (2% and 4% end‐tidal) lowered the arterial pressure of the pithed rat. Heart rate was increased by diethyl ether 4%, decreased by halothane and unchanged by cyclopropane.
While each anaesthetic depressed the pressor responses to sympathetic nerve stimulation, cyclopropane increased and halothane and diethyl ether depressed the pressor responses to exogenous noradrenaline.
Each anaesthetic reduced the motor responses of the smooth muscle of the colon to parasympathetic stimulation.
The significance of the effects on peripheral neuroeffector systems is discussed in relation to the overall circulatory changes produced by these anaesthetics in the whole animal.
REPEATED EXPOSURE OF RATS TO THE CONVULSANT AGENT FLUROTHYL ENHANCES 5‐HYDROXYTRYPTAMINE‐ AND DOPAMINE‐MEDIATED BEHAVIOURAL RESPONSES
Authors: GREEN A.R. 
Published: July 2012

Rats were convulsed once daily for 7 days by exposure to the inhalant convulsant agent, flurothyl (Indoklon, bis (2,2,2‐trifluouroethyl)ether). Twenty four hours after the final convulsion the rats were injected with tranylcypromine (20 mg/kg) followed 30 min later by L‐DOPA (50 mg/kg), a procedure which increases brain dopamine concentrations. The flurothyl‐treated rats showed a greater locomotor activity response than rats that had not been convulsed.
This enhanced response appears to be due to increased postsynaptic dopamine receptor sensitivity since flurothyl‐treated rats also showed enhanced locomotor responses to methamphetamine (2 mg/kg) and apomorphine (2 mg/kg).
Enhanced 5‐hydroxytryptamine‐induced activity responses following administration of tranylcypromine (20 mg/kg) and L‐tryptophan (50 mg/kg) were also seen 24 h after the last of 10 daily flurothyl‐induced convulsions.
The increased 5‐hydroxytryptamine response also appears to be due to increased postsynaptic sensitivity since the flurothyl‐treated rats showed increased hyperactivity following administration of tranylcypromine (20 mg/kg) and the suggested 5‐hydroxytryptamine agonist, 5‐methoxy N,N‐dimethyltryptamine (2 mg/kg).
No change in the brain concentration of 5‐hydroxytryptamine, 5‐hydroxyindoleacetic acid, tryptophan, dopamine or noradrenaline was observed 24 h after the last of 10 daily flurothyl‐induced convulsions, compared to untreated rats. The rate of 5‐hydroxytryptamine accumulation after tranylcypromine/L‐tryptophan treatment and of dopamine and noradrenaline accumulation after tranylcypromine/L‐DOPA treatment was similar in both groups.
Repeated flurothyl convulsion has the same effects on these behavioural tests as repeated electro‐convulsive shock. Since both treatments have been used successfully to treat depression, it is suggested that the mechanism of action of electroconvulsive therapy may be by increasing postsynaptic responses to the monoamine neurotransmitters.
H1‐ AND H2‐RECEPTORS IN THE SMOOTH MUSCLE OF THE RUMINANT STOMACH
Authors: OHGA A. , TANEIKE T. 
Published: July 2012

The effects of histamine on the longitudinal and circular smooth muscle from the rumen and reticulum of the bovine stomach have been analyzed by the use of H1‐ and H2‐receptor antagonists.
Histamine caused three different types of response of the smooth muscle preparations: a contraction, contraction followed by relaxation, and a relaxation. These responses were resistant to the effect of tetrodotoxin, atropine, combined treatment with α‐ and β‐ adrenoceptor blocking agents, hexamethonium and also to guanethidine.
Mepyramine antagonized the contractile responses and metiamide antagonized the relaxation responses in a highly selective and competitive manner.
It is concluded that histamine‐induced excitatory and inhibitory responses of the smooth muscles from the bovine forestomach are mediated by histamine H1‐ and H2‐receptors, respectively.