bluuebunny/crossref_metadata_2025_split huggingface dataset:
EFFECT OF SODIUM INTAKE ON INTRAERYTHROCYTE SODIUM CONCENTRATION IN NORMOTENSIVE SUBJECTS AND PATIENTS WITH UNTREATED MILD HYPERTENSION
Authors: Myers J. B. , Morgan T. O. , Edwards K. 
Published: June 2007

SUMMARY1. The effect of changing sodium intake for 2 weeks was studied. Twelve nor‐motensive subjects and five patients with mild essential hypertension were given two different levels of sodium intake for 2 weeks.2. Overall there was no significant rise in blood pressure but all patients with hypertension had a rise in blood pressure as they went from a low to a high sodium intake.3. Plasma sodium was not altered but red cell sodium concentration was higher on the high sodium intake. This effect was observed in both normotensive and hypertensive people.4. Alterations observed in cell sodium concentration provide support for the hypothesis that increased dietary intake of sodium may induce hypertension by causing changes in cellular transport systems.
PRESSOR EFFECT OF MODERATE ALCOHOL CONSUMPTION IN MAN: A PROPOSED MECHANISM
Authors: Ireland Mark , Vandongen Robert , Davidson Lisa , Beilin Lawrence , Rouse Ian 
Published: June 2007

SUMMARY1. Ingestion of alcohol was associated with a highly significant increase in systolic blood pressure and heart rate which occurred before the blood alcohol reached its peak concentration of 16.9 (s.e.m. = 1.1) mol/1.2. Drinking non‐alcoholic cold liquids caused a marked but transient fall in adrenaline and a rise in noradrenaline concentration.3. Alcohol prevented this fall in adrenaline and led to a sustained increase in noradrenaline concentration.4. These changes may be implicated in the elevation of blood pressure associated with alcohol consumption.
EFFECTS OF IMIPRAMINE ON THE ORTHOSTATIC CHANGES IN BLOOD PRESSURE, HEART RATE AND PLASMA CATECHOLAMINES
Authors: Nielsen Jens Rokkedal , Johansen Torben , Arentoft Anne , Gram Lars F. 
Published: June 2007

SUMMARY2. Imipramine caused a moderate increase in supine systolic blood pressure, and a pronounced increase in the rise in heart rate, when the subjects assumed erect position.3. The orthostatic drop in systolic blood pressure was in most cases only moderately increased after ingestion of imipramine, but in three subjects pronounced orthostatic hypotension developed when the sodium balance was low, whereas no clinical symptoms were seen in the same subjects when tested after imipramine ingestion on a high sodium balance.4. The plasma catecholamine levels in supine and standing position were not influenced by imipramine or by the changes in sodium balance.5. The data may suggest that inhibition of presynaptic reuptake of noradrenaline and/or α‐adrenoceptor blockade causes the moderate rise in supine blood pressure, whereas α,‐adrenoceptor blockade, mainly affecting the venous part of the vascular bed, may explain the orthostatic reactions.
ANTAGONISM BY MANGANESE OF ISOPRENALINE DILATATION OF THE GUINEA‐PIG ISOLATED TRACHEA
Authors: Jamieson Dana D. , Quinnf R. J. , le Coutier A. 
Published: June 2007

SUMMARY1. Manganese (0.5‐100 μmol/1) was found to be a potent inhibitor of the dilator effect of isoprenaline on the isolated tracheal muscle of the guinea‐pig. Above these concentrations the inhibitory action of Mn2+ diminished and no inhibition occurred above 1000 μmol/I Mn2+. Thus a bell‐shaped dose‐response curve resulted for the inhibition of isoprenaline by Mn2+. The antagonism was surmountable but apparently noncompetitive.2. Dilation of the isolated trachea caused by theophylline or nitroprusside was not inhibited by Mn2+ at concentrations of 12.5 to 750 μmol/1.3. At the dose range which could be tested manganese did not antagonize isoprenaline bronchodilatation in vivo. However, manganese at doses between 0.5 and 2.0 μmol/kg inhibited increases in pulmonary resistance caused by acetylcholine, histamine or serotonin.4. At concentrations above 250 μmol/1 Mn2+ inhibited constrictor responses to histamine, acetylcholine and serotonin in guinea‐pig isolated ileum and trachea, and inhibited serotonin and prostaglandin E2 contractions in rat fundus.5. Co2+, Fe2+, Fe3+ and Zn2+ were also tested for their action against isoprenaline on the isolated trachea. Co2+ was similar in effect to Mn2+ but had only 1/50 of the potency. Up to the highest concentrations which could be tested, namely 1000 μmol/1, the other trace metals produced negligible effects.6. Thus Mn2+ showed selective inhibition of the relaxant effect of isoprenaline on the guinea‐pig isolated trachea, at concentrations of Mn2+ well below those shown previously to inhibit constrictor responses by block of transmembrane Ca2+ entry. It is suggested that Mn2+ may interfere with intracellular Ca2+ fluxes in the isolated trachea.
PRESYNAPTIC INHIBITION BY SEROTONIN OF CARDIAC SYMPATHETIC TRANSMISSION IN DOGS
Authors: Kimura T. , Satoh S. 
Published: June 2007

SUMMARY1. The effect of serotonin on cardiac sympathetic transmission was investigated in vagotomized and cardiac decentralized dogs.2. Administration of serotonin in doses of 10‐100 μg/kg i.v., during the resting unstimulated state caused tachycardia and pressor responses which were inhibited by cyproheptadine but not by guanethidine. The tachycardia was reduced by a β‐adrenoceptor antagonist, bufetolol.3. Serotonin in doses of 3‐100 μg/kg depressed the elevated heart rate during maintained electrical stimulation of the cardiac sympathetic nerves.4. Cyproheptadine did not antagonize the serotonin‐induced depression of the stimulation‐elevated heart rate, while desipramine attenuated but did not abolish it.5. Serotonin did not have a significant effect on the heart rate elevated by maintained infusion of noradrenaline.6. The present results suggest that serotonin‐induced depression of heart rate during sympathetic nerve stimulation is due to presynaptic inhibition by serotonin of cardiac sympathetic transmission which is not mediated via‘classic’ tryptaminergic receptors.
INFLUENCE OF FLA‐63 ON PENTOBARBITONE SLEEP IN CHICKS AND RATS
Authors: Wambebe C. , Osuide G. 
Published: June 2007

SUMMARY1. The influence of FLA‐63 on pentobarbitone‐induced sleep was studied in young chicks and adult rats.2. FLA‐63 produced a time‐dependent biphasic effect on the gross behaviour of chicks and rats; an initial sedation followed by behavioural excitation.3. The behavioural effects of FLA‐63 were associated with an initial EEG synchronization prior to an increased activity of the EMG of the neck muscle and desynchronization of the EEG of the hyperstriatum, optic tectum and pontine reticular formation of the chick. Similarly, in rats, the EEG of the frontal cortex, optic lobe and pontine reticular formation was desynchronized while the EMG activity of the neck muscle was enhanced by FLA‐63.4. FLA‐63 delayed the onset and shortened the duration of pentobarbitone sleep.5. Pentobarbitone‐induced EEG synchronization and decreased EMG activity in chicks was antagonized by FLA‐63.6. Dopamine‐induced antagonism of pentobarbitone sleep was potentiated by FLA‐63 in chicks.7. Levodopa antagonized pentobarbitone‐induced sleep in rats and this effect was potentiated by FLA‐63.8. FLA‐63 potentiated levodopa‐induced desynchronization of the EEG of the frontal cortex, optic lobe and pontine reticular formation of the rat.9. Haloperidol antagonized the effect of FLA‐63 on pentobarbitone‐induced sleep in both rats and chicks.10. Noradrenaline induced behavioural sleep in young chicks dose‐dependently; this effect was antagonized by phentolamine. In the rat, phentolamine shortened pentobarbitone sleeping time but did not significantly influence the effects of FLA‐63 on pentobarbitone sleep.11. Those results suggest that an increased dopamine neurotransmission may be associated with the mechanism of wakefulness in chicks and rats.
TRIFLUOPERAZINE ANTAGONIZES INHIBITION OF RENIN RELEASE BY ANGIOTENSIN II
Authors: Schwertschlag Ullrich , Hackenthal Eberhard 
Published: June 2007

SUMMARY1. The influence of trifluoperazine (TFP) treatment on angiotensin H‐induced inhibition of renin release from the rat isolated perfused kidney was examined. Angiotensin II, 1 /imol/1, in the presence of 1 mmol/1 calcium, reduced basal renin secretion by 70%. When calcium was omitted from the perfusion medium, inhibition of renin release no longer occurred. Pretreatment of the rat isolated perfused kidney with the calmodulin inhibitor trifluoperazine (TFP), 10 μmol/1 for 6 min, interfered with the inhibitory action of angiotensin II on renin release as well as angiotensin II‐induced renal vasoconstriction. Our data suggest a role for calmodulin in mediating the effects of angiotensin II on both renin release and renal vascular resistance.
URINARY EXCRETION OF GLYCOSAMINOGLYCANS, HYDROXYPROLINE AND HYDROXYLYSINE IN RABBITS AFTER EXCESSIVE INGESTION OF FLUORIDE
Authors: Jha Mohan , Koacher Jasbeer , Susheela A. K. 
Published: June 2007

SUMMARY1. Urinary levels of glycosaminoglycans (GAG) and hydroxyproline from normal and fluoride treated rabbits were estimated. The hydroxylysine content of serum and urine of rabbits after excessive ingestion of fluoride was also investigated.2. There was a progressive decrease in GAG content, reduction in hydroxylysine, whereas the hydroxyproline content was increased after fluoride ingestion.3. Enhanced hydroxyproline in urinary excretion is due to collagen breakdown after fluoride ingestion.4. The reduction in hydroxylysine content is due to reduced collagen cross‐link formation.5. The report suggests the possibility of using the urinary levels of GAG or hydroxyproline or hydroxylysine as an index of fluoride intoxication.
PHARMACOKINETICS OF AN OSMOTICALLY CONTROLLED DELIVERY INDOMETHACIN PREPARATION IN NORMAL VOLUNTEERS
Authors: Bertouch J. V. , Maycock S. , Harrington B. , Brooks P. M. 
Published: June 2007

SUMMARYIndomethacin is still used commonly for the treatment of rheumatic diseases but is associated with side effects, particularly headache, in a number of patients. A controlled or sustained release formulation of indomethacin might provide lower peak plasma levels and thus reduce side effects while still maintaining adequate plasma levels to control pain and inflammation.In this single dose crossover study, normal volunteers received the new formulation of indomethacin (Indocid GITS 6/85) fasting or with a standard meal, indomethacin 75 mg with a standard meal or indomethacin 25 mg three times daily with a standard meal.Plasma concentration data showed that peak plasma levels were reduced but the area under the plasma concentration curve was not significantly different between the four treatments.
INFLUENCE OF SEASON AND ANAESTHETIC ON CUTANEOUS VASCULAR PERMEABILITY RESPONSES TO HISTAMINE, SEROTONIN AND MAST CELL‐RELEASING AGENTS IN RATS
Authors: Chahl Loris A. 
Published: June 2007

SUMMARYThe influences of season and anaesthetic on the cutaneous vascular permeability responses to histamine (2.5 × 10−8 mol), serotonin (5HT, 2.5 × 10−10 mol), and to the mast cell‐releasing agents adenosine 51‐triphosphate (2.5 × 10−7 mol), dextran (5 × 10−5 g) and compound 48/80 (1 × 10−7 g) were examined using an Evans blue dye leakage technique.In rats anaesthetized with urethane (1 g/kg i.p.), responses to irritants were significantly less than in rats given ether for the period of administration of irritants and allowed to recover consciousness. The response to histamine was mediated by Hi‐receptors since it was abolished by mepyramine but not by metiamide.The only seasonal variation observed was in responses to 5HT in urethane‐anaesthetized rats, which were significantly less in winter than in summer. It was concluded that dye leakage responses to irritants are affected more by anaesthetic than by seasonal variation.
LEAKAGE OF CATECHOLAMINES FROM RABBIT CEREBROSPINAL FLUID FOLLOWING INTRACEREBROVENTRICULAR INJECTION
Authors: Maccarrone C. , Malta E. , Raper C. 
Published: June 2007

SUMMARY1. The intracerebroventricular (i.c.v.) injection of (‐)‐isoprenaline and the selective β1‐adrenoceptor agonist, RO363, elicited reproducible dose‐related increases in heart rate in unanaesthetized and anaesthetized rabbits. (‐)‐Isoprenaline produced vasodepressor effects in unanaesthetized animals, whereas both catecholamines decreased blood pressure in anaesthetized rabbits.2. Pretreatment with guanethidine sulphate (5 mg/kg i.v.) reduced but did not abolish the tachycardia elicited by i.c.v. RO363, whereas heart rate responses to i.c.v. (‐)‐isoprenaline were unaffected.3. Pretreatment of anaesthetized rabbits with hexamethonium bromide (10 mg/kg i.v.) did not markedly affect the tachycardia elicited by i.c.v. RO363 and reduced the response to i.c.v. (‐)‐isoprenaline in only one out of five experiments.4. The results suggest that there is a marked leakage of centrally administered catecholamines into the peripheral circulation and that the rabbit may be unsuited for examining centrally mediated cardiovascular effects of catecholamines.
MUSCARINIC RECEPTOR INHIBITION AND OTHER EFFECTS OF PANCURONIUM IN THE RABBIT EAR ARTERY PREPARATION
Authors: Leung E. , Mitchelson F. 
Published: June 2007

SUMMARY1. The effect of pancuronium in the rabbit ear artery was investigated in order to measure the inhibition it produces at the prejunctional muscarinic receptor on sympathetic nerve endings in this tissue.2. Pancuronium (0.1–0.2 mmol/l) produced an enhancement of responses to transmural electrical stimulation but this effect was absent in experiments conducted in the presence of cocaine (10 μmol/l) suggesting that an inhibition of the uptake, mechanism occurs with pancuronium in this tissue.3. Pancuronium (10 μmol/l) in the presence of cocaine (10 μmol/l) and yohimbine (1 μmol/l) caused a small transient increase in resting output of tritium from arteries preincubated with 3H‐noradrenaline but did not affect stimulated output of tritium nor the perfusion pressure in perfused preparations.4. Pancuronium in the presence of cocaine or cocaine plus yohimbine caused a parallel shift of the concentration‐response curve for the inhibitory effect of carbachol (CCh) on the increase in perfusion pressure induced by nervous stimulation. An Arunlakshana‐Schild plot of the data was linear but the slopes of 0.92 and 0.95 respectively, were significantly different from unity (P<0.05).5. The calculated pKB value suggests that pancuronium has a different affinity for prejunctional muscarinic receptors on sympathetic nerve endings in this tissue compared to that previously reported in cardiac or ileal smooth muscle.
ACTIONS OF INDORAMIN ON RABBIT AND HUMAN VASCULATURE IN VITRO
Authors: Black J. L. , Mylecharane E. J. 
Published: June 2007

SUMMARY1. The antagonist effects of indoramin were investigated in rabbit perfused ear artery, common carotid artery, and human perfused temporal artery preparations.2. Indoramin was a potent competitive antagonist of the constrictor effects of noradrenaline (NA) in all three preparations, pA2 values being 7.77 for the ear artery, 8.20 for the common carotid artery and 7.46 for the human temporal artery.3. The constrictor actions of serotonin (5‐hydroxytryptamine, 5‐HT) were competitively antagonized by indoramin. The pA2 values obtained in the rabbit common carotid and human temporal artery (5.92 and 6.25, respectively), were lower than those for NA in the same preparations and lower than that obtained in the rabbit perfused ear artery (7.55).4. Indoramin was a potent competitive antagonist (pA2:8.31) of histamine‐induced vasoconstriction in the rabbit perfused ear artery preparation.5. These results can be explained on the basis of previous findings that the action of 5‐HT in the rabbit ear artery is mediated via an α‐adrenoceptor, and that the rabbit common carotid artery contains true 5‐HT receptors. The findings suggest that specific 5‐HT receptors may be present in the human temporal artery and that α‐adrenoceptor antagonism may be the pharmacological property of most relevance to the efficacy of indoramin in migraine prophylaxis.
IMPORTANCE OF CENTRAL SEROTONIN NEURONS IN THE HYPOTENSIVE ACTION OF METHYLDOPA IN THE RAT
Authors: Choy Vernon J. , Chalmers John 
Published: June 2007

SUMMARY1. Normotensive (WKY) and stroke prone spontaneously hypertensive (SHR‐SP) rats were given methyldopa (200 mg/kg i.p.) daily for five days and their brains were then sectioned and processed with the Faglu method for catecholamine fluorescence.2. This treatment with methyldopa induced a green fluorescence not seen in control animals, in cells coinciding with the B1–B9 groups of serotonin neurons in the brainstem.3. Pretreatment with the neurotoxin 5,7‐dihydroxytryptamine (5,7‐DHT, i.c.v.), which is relatively specific for serotonin neurons, prevented the appearance of this green fluorescence in the serotonin cell groups of rats given methyldopa.4. Pretreatment with 5,7‐DHT, i.c.v. approximately halved the magnitude of the hypotensive response to a single dose of methyldopa (80 mg/kg i.p.).5. We suggest that central serotonin nerves contribute to the hypotensive action of methyldopa.6. It is our hypothesis that methyldopa is taken up by these serotonin cells and that the green fluorescence reflects the production of α‐methyldopamine, as a result of decarboxylation by the ubiquitous enzyme, L‐aromatic amino acid decarboxylase.
EFFECTS OF HISTAMINE AND HISTAMINE ANTAGONISTS ON HEPATIC BILE FLOW IN THE CONSCIOUS SHEEP
Authors: Lee S. P. 
Published: June 2007

SUMMARY1. The effects of histamine and histamine antagonists on bile flow have been studied using the cholecystectomized conscious sheep. Histamine stimulated bile flow in a dose‐dependent manner (D50= 15.7 μg/h per kg). Free water and HCO3− output were increased after intravenous histamine infusion. With histamine at 120 mg/h per kg, there was a 41.0 (s.d. = 4.6)% and 38.7 (s.d. = 4.2)% (n= 6) increase in bile volume and HCO3− output respectively. Bile salt concentration was decreased after intravenous histamine, but net bile salt secretory rate remained unchanged. There was no change observed in the molar ratios of bile salts:phospholipids:cholesterol. Total lipids were decreased from 2.2 (s.d. = 0.3) to 1.60 (s.d. = 0.4) g/dl (n=6). The corrected lithogenic index did not change significantly. 14C‐Erythritol clearance also increased during histamine infusion in a dose‐dependent manner but did not correspond to increments in bile flow.2. The histamine H1‐receptor antagonist, diphenhydramine 0.05–1.0 mg/h per kg did not alter histamine stimulated bile flow. The H2‐receptor antagonists, cimetidine (0.5–4 mg/h per kg) and ranitidine (0.05–0.5 mg/h per kg) progressively reversed the histamine‐induced choleresis. Maximum inhibitory effect was attained at 2.0 and 0.25 mg/h per kg for cimetidine and ranitidine, respectively. At these levels, variation of intravenous infusion of histamine did not result in competitive displacement of the inhibitory response by either cimetidine or ranitidine. Moreover, concomitant infusion of diphenhydramine at 1.0 mg/h per kg potentiated the inhibitory effect of cimetidine or ranitidine on histamine‐induced choleresis.3. Histamine increases the bile salt independent component of hepatic bile flow. This increase can be blocked by cimetidine or ranitidine by a non‐competitive inhibitory mechanism.
EFFECT OF ACTH ADMINISTRATION ON URINARY KALLIKREIN EXCRETION IN MAN
Authors: Whitworth Judith A. , van Leeuwen Barbara H. , Hannah Murray C. , Scoggins Bruce A. , Thatcher Robin 
Published: June 2007

SUMMARY1. The effect of ACTH administration on urinary kallikrein excretion and its relationship to changes in plasma and urine electrolytes, renin concentration and steroids was examined in normotensive and mildly hypertensive subjects.2. ACTH administration produced hypokalaemia, initial urinary sodium retention, a fall in active plasma renin concentration, a transient rise in plasma aldosterone concentration and sustained rises in plasma deoxycorticosterone concentration and urinary kallikrein activity.3. Changes in patients with mild hypertension were similar in pattern to normotensives, but urinary kallikrein concentrations were lower.4. The effects of ACTH on urinary kallikrein excretion appeared to be independent of aldosterone and correlated most closely with deoxycorticosterone concentrations.
PRESENCE OF CHOLINOCEPTORS IN MESENCEPHALIC RAPHE NUCLEI CONCERNED IN THERMOREGULATION IN RABBITS
Authors: Saxena A. K. , Tangri K. K. , Mishra Nisha , Vrat S. , Bhargava K. P. 
Published: June 2007

SUMMARY1. The thermal effects of cholinomimetics and cholinoceptor blocking agents microinjected into mesencephalic nucleus raphe medianus (NRM) were investigated in rabbits to determine the nature and role of these cholinoceptors in thermoregulation.2. Microinjection of cholinoceptor agonists, carbachol and pilocarpine, into NRM resulted in significant hyperthermia which could be blocked by local pretreatment with chlorisondamine (a nicotinic receptor blocker) as well as by ethybenztropine (a muscarinic receptor blocker).3. Intracerebroventricular pretreatment with LM 5008 (serotonin reuptake blocker) significantly inhibited the carbachol‐induced hyperthermia.4. Both nicotinic and muscarinic cholinoceptors are present in mesencephalic NRM which may be involved in thermoregulation in rabbits. Activation of these cholinoceptors in NRM results in hyperthermia which seems to be due to an inhibition of a serotonin sensitive hypothalamic heat loss mechanism.
RELATIVE CONTRIBUTIONS OF VAGAL AND CARDIAC SYMPATHETIC NERVES TO THE REFLEX BRADYCARDIA INDUCED BY A PRESSOR STIMULUS IN THE CONSCIOUS RABBIT: COMPARISON OF ‘STEADY STATE’ AND ‘RAMP’ METHODS
Authors: Weinstock Marta , Rosin A. J. 
Published: June 2007

SUMMARY1. The bradycardic response to a pressor stimulus, phenylephrine, was studied simultaneously in conscious rabbits by two different methods.2. The ‘steady state’ method, in which bradycardia was measured at the peak of each pressor stimulus, demonstrated the existence of two groups of animals, in which the maximal heart periods were 867 (s.e.m. =49) and 563 (s.e.m. =34) ms and the slopes of the MAP‐HP relationship were 24.6 (s.e.m. =1.6) and 8.1 (s.e.m. =0.7) ms/mmHg, respectively.3. The difference in baroreflex sensitivity in the two groups was abolished by sympathetic nerve blockade with guanethidine (10 mg/kg) but not by vagal blockade.4. The ‘ramp method’ which measures bradycardia during the rapid phase of MAP rise after phenylephrine did not detect any difference in response of the two groups of rabbits.5. Guanethidine did not alter the slope of the MAP‐HP relationship in either group of rabbits when this was assessed by the ‘ramp’ method.6. These findings demonstrate that the ‘steady state’ method can detect changes in both vagal and sympathetic activity, while the ‘ramp’ method measures only vagally induced bradycardia.7. It is concluded that some rabbits may have a genetic ability to activate baroreflex pathways mediating cardiac sympathetic inhibition in addition to vagal stimulation in response to a pressor stimulus.