bluuebunny/crossref_metadata_2025_split huggingface dataset:
CONTROLLED STUDY OF THE EFFECTS OF DIETARY PROTEIN ON BLOOD PRESSURE IN NORMOTENSIVE HUMANS
Authors: Prescott S. L. , Jenner D. A. , Beilin L. J. , Margetts B. M. , Vandongen R. 
Published: June 2007

SUMMARY1. The object of this study was to determine whether meat protein per se is responsible for the higher blood pressures (BP) in omnivores compared with vegetarians.2. Assessments were made by a double blind randomized control trial in 64 normo‐tensive volunteers recruited from Royal Perth Hospital staff.3. All volunteers were given a ‘meat’ substitute during the 2 week control period. Randomization was then introduced into two dietary groups: the first remained on the ‘meat’ substitute, and the other received a ‘non‐meat’ substitute of vegetable protein, for the remaining 12 weeks of the trial.4. The content of ‘meat’ and ‘non‐meat’ substitute was designed quantitatively and qualitatively to represent the protein intake in recently studied diets of Australian omnivores and ovo‐lacto vegetarians, respectively. The levels of fats (saturated and unsaturated), fibre, energy, Na+, K+, Mg2+, Ca2+ and carbohydrate in the intervention diets were similar.5. These dietary changes were not associated with any significant changes in BP. Significantly lower urinary 3‐methyl histidine excretions in volunteers receiving ‘non‐meat’ supplements compared with the ‘meat’ eaters confirmed the dietary changes.6. It was concluded that BP differences between omnivores and accultured vegetarians are unlikely to be due to differences in protein intake.
CAN THE SYNTHESIS OF PLATELET‐ACTIVATING FACTOR, A POTENT VASODILATOR AND PRO‐AGGREGATORY AGENT, BE ALTERED BY DIETARY MARINE OILS?
Authors: Codde James P. , Vandongen Robert , Mori Trevor A. , Beilin Lawrence J. , Hill Kathryn J. 
Published: June 2007

SUMMARY1. Diets enriched with n‐3 polyunsaturated fish oils, predominantly eicosapen‐taenoic acid, are associated with a lower risk of atherosclerotic vascular disease. These oils purportedly reduce plasma triglycerides, total cholesterol and impair platelet aggregation. Recently, the present authors reported that rats fed a marine oil‐enriched diet had significantly reduced levels of lyso‐PAF, the immediate precursor of platelet‐activating factor (PAF). As PAF has potent vasodilator and pro‐aggregatory properties, the purpose of this study was to examine the hypothesis that fish oils affect the biosynthesis of PAF in man.2. Supplementation of a normal diet for 3 weeks with fish oil containing the equivalent of 2.7 g of eicosapentaenoic acid daily, increased the eicosapentaenoic acid content of platelet phospholipids as well as depleting the arachidonic acid. Platelet aggregation to PAF (measured in whole blood by impedance aggregometry) was significantly impaired and whole blood thromboxane suppressed.3. Two weeks after ceasing supplements, platelet aggregation remained impaired although thromboxane had reverted to baseline levels. There was a transient but significant fall in whole blood lyso‐PAF apparent within 2 days of commencing supplements but returning to baseline levels by the end of the treatment period. Whole blood PAF followed a similar trend.4. The effects of dietary fish oil on whole blood aggregations to PAF, on thromboxane and plasma lyso‐PAF levels may be relevant to the prevention of vascular disease and the treatment of disorders in which PAF could be an inflammatory mediator.
ATRIAL NATRIURETIC FACTOR IN CHRONIC RENAL FAILURE: STUDIES IN MAN AND THE RAT
Authors: Hodsman G. P. , Jackson B. , Debrevi L. M. , Ogawa K. , Johnston C I. 
Published: June 2007

SUMMARY1. Plasma concentration and atrial content of atrial natriuretic factor (ANF) were measured in rats with chronic renal failure induced by subtotal nephrectomy.2. Plasma ANF was higher, and atrial ANF content lower in rats with renal failure when compared with sham‐operated controls.3. Plasma renin activity (PRA) and ANF were elevated at 1 week following subtotal nephrectomy. After 1 month plasma ANF had risen further, but PRA was suppressed to below control values.4. Plasma ANF was also measured in six patients with chronic renal failure undergoing routine haemodialysis.5. Elevated plasma ANF levels in patients with renal failure were lowered by haemodialysis, although extraction of ANF across the dialysis membrane was negligible.6. Secretion of ANF is increased in chronic renal failure in man and the rat, possibly mediated by increased intravascular volume.
EFFECTS OF NEUROPEPTIDE Y ON LEFT VENTRICULAR FUNCTION IN THE CONSCIOUS RABBIT
Authors: Minson R. B. , McRitchie R. J. , Chalmers J. P. 
Published: June 2007

SUMMARY1. Changes in arterial pressure, heart rate and left ventricular contractility induced by intravenous injections of neuropeptide Y (NPY; 1–30 μg/kg) were studied in the conscious rabbit.2. NPY has a brief pressor effect associated with a bradycardia, an increase in left ventricular end diastolic pressure, and a prolonged fall in peak left ventricular dP/dt (LVdP/dt).3. The haemodynamic changes increase substantially with increasing doses up to 10 μg/kg. Beyond 10 μg/kg there are only slight effects on heart rate or peak LV dP/dt.
AIRWAY RESPONSES IN VITRO FOLLOWING C5A DES ARG‐INDUCED HYPER‐RESPONSIVENESS IN VIVO IN RABBITS
Authors: Armour C. L. , Black J. L. , Vincenc K. S. , Johnson P. R. A. , Ward H. , Berend N. 
Published: June 2007

SUMMARY1. The mechanism of C5a des Arg‐induced airway hyper‐responsiveness in rabbits was investigated.2. Airway smooth muscle from rabbits which had been pretreated in vivo, was studied in vitro. Tracheal rings, segmental bronchial rings, subsegmental bronchial spirals and lung parenchymal strips were all prepared from each rabbit lung.3. Although C5a des Arg produces hyper‐responsiveness to histamine in vivo, which is inhibited by indomethacin, the airway smooth muscle responses in vitro from control, C5a des Arg and C5a des Arg plus indomethacin pretreated rabbits did not differ.4. The neutrophil counts in the tracheal and subsegmental bronchial specimens were increased in the C5a des Arg‐treated group. Indomethacin significantly (P<0.05) inhibited the neutrophil influx in the subsegmental bronchi.5. It is concluded that intrinsic smooth muscle function is unaltered following C5a des Arg‐induced hyper‐responsiveness in vivo.
THE EFFECT OF CORTICOSTEROID PRETREATMENT IN VIVO ON THE CONTRACTION OF GUINEA‐PIG ILEUM AND DUODENUM
Authors: Morat Paden , Khalid B. A. K. , Merican Z. , Idid S. Z. , Alias A. K. 
Published: June 2007

SUMMARY1. The effects of corticosteroid pretreatment on the contraction caused by acetylcholine or electrical stimulation of guinea‐pig ileum and duodenum were studied.2. The acetylcholine dose‐response curves for steroid pretreated ileum but not duodenum were significantly shifted to the right; evidence that pretreated ileum required higher dose of acetylcholine than normal to cause 50% maximal contraction.3. Naloxone enhanced the contraction of normal ileum caused by acetylcholine given at the dose of ED50, but not that of normal duodenum.4. The dose of morphine required to abolish electrically induced contraction was higher in steroid pretreated ileum than in normal ileum.5. Hence, corticosteroid pretreatment may affect intestinal contractility via opioidergic mechanisms which are found in the ileum but not in the duodenum.
HIGH‐AFFINITY ALDOSTERONE BINDING IN RAT LIVER—A RE‐EVALUATION
Authors: Zaini Anuar , Pearce Paul , Funder John W. 
Published: June 2007

SUMMARY1. The use of sodium molybdate as a stabilizing agent, and a RU26988 to exclude [3H]aldosterone from Type II glucocorticoid receptors, has enabled us to characterize high affinity Type I aldosterone binding sites in rat liver cytosol.2. In liver cytosols from male rats aldosterone bound with an affinity (Kd‐22°C) of 0.6 nmol/l (range 0.3–0.8 nmol/l), and Nmax 1.7 fm/mg protein (s.e.m. = 0.4); specificity of binding was similar to that for Type I sites in classical aldosterone target tissues (aldosterone ≥ corticosterone > dexamethasone).3. Hepatic Type I receptor levels were relatively constant in both male and female rats aged 30–120 days, with levels significantly higher in females.4. Parallel studies on hepatoma H4 cells showed levels of Type I sites similar to those in normal liver, suggesting a general distribution of such sites throughout liver parenchyma, rather than a concentration in a specific cell type.5. The function of such Type I sites, and whether or not they are aldosterone‐selective in vivo and can thus act as mineralocorticoid receptors, remains to be determined.
PLASMA ATRIAL NATRIURETIC PEPTIDE IS INCREASED DURING ATRIAL PACING IN CONSCIOUS RABBITS
Authors: Morris M. J. , Pilowsky P. M. , Cain M. D. , Chalmers J. P. 
Published: June 2007

SUMMARY1. The effect of increases in heart rate on plasma atrial natriuretic peptide (ANP) concentrations was investigated in conscious rabbits.2. Plasma ANP concentrations were significantly increased following abrupt increases in heart rate produced by atrial pacing at 400 beats/min. Pacing at 300 beats/min resulted in smaller increases in plasma ANP concentration.3. Stepwise increases in heart rate produced by atrial pacing at 250, 300, 350 and 400 beats/min resulted in increases in plasma ANP concentrations at 400 beats/min only.4. The increase in plasma ANP concentration during atrial pacing correlated significantly with the increase in heart rate achieved.
INVOLVEMENT OF SYMPATHETIC NERVOUS SYSTEM INHIBITION IN THE HYPOTENSIVE EFFECT OF BROMOCRIPTINE IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kanayama Y. , Kohno M. , Takaori K. , Itoh S. , Yasunari K. , Takeda T. 
Published: June 2007

SUMMARYThe hypertensive effect of bromocriptine in young (6 week old) spontaneously hypertensive rats (SHR) was studied. Blood pressure and plasma norepinephrine level in bromocriptine‐treated SHR were significantly lower than those in vehicle‐treated SHR after 3 weeks of treatment (5 mg/kg per day, i.p.), while no significant decrease of blood pressure or plasma norepinephrine level was observed after 2 weeks of treatment. These results suggest the involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in SHR.
AMANTADINE RESTORES IMPULSE CONDUCTION ACROSS DEMYELINATED NERVE SEGMENTS
Authors: Schauf C. L. 
Published: June 2007

SUMMARY1. Drugs can be identified that relieve clinical symptoms of demyelinating diseases such as multiple sclerosis based on their ability to alter voltage‐dependent ion channels in membranes and restore conduction in demyelinated nerve. Beneficial drugs either slow inactivation of membrane Na+ channels or block K+ channels.2. Amantadine, an antiviral drug that slows Na+ inactivation in Myxicola giant axons, restores conduction in frog and rat sciatic nerves partially demyelinated by disruption of the perineurium (the ‘perineurial window') loose ligatures, or lysolecithin.3. A positive effect of amantadine on several different animal models supports the need for clinically oriented studies of amantadine and related inactivation‐blocking agents in diseases such as multiple sclerosis.
SYMPATHETIC NERVOUS SYSTEM MEDIATES URINARY KALLIKREIN EXCRETION IN CONSCIOUS RATS
Authors: Albertini R. , Vargas L. , Oliveri P. , Pardo F. , Paredes M. C. 
Published: June 2007

SUMMARY1. The influence of the sympathetic nervous system on urinary kallikrein excretion (UKal) was investigated in conscious rats during stress produced by inserting a silastic catheter through the urethra into the bladder. The effect of this stress on blood glucose (BG), mean arterial pressure (MAP), urinary volume (Uv), urinary sodium (UVNa), and glomerular filtration rate (GFR) was also studied.2. In intact animals stress of 120 min duration produced a non‐significant increase of MAP, a significant increase of BG and a decrease of UNa (P < 0.001 t‐test, 9 d.f.), but it did not affect Uv and GFR. In stressed rats UKal was considerably lower (52 milli Amidasic Units [mAU] per 100 g bodyweight, s.e.m. = 5, n= 6) than in control rats (170 mAU per 100 g, s.e.m. = 21, n= 5). The inhibitory effect on UKal was also observed when kallikrein was measured by the kininogenase method.3. Adrenal medullectomy, performed 1 week before the experiment, suppressed the stress hyperglycaemia but did not affect the reduction of urinary kallikrein or the anti‐natriuresis.4. Intracerebroventricular (i.c.v.) injection of saline also had no effect in the control or in the stressed rats, while i.c.v. d‐l‐propranolol decreased MAP, suppressed the stress hyperglycaemia and the anti‐natriuresis and stimulated UKal, without changes in Uv and GFR. Non‐stressed control rats i.c.v. injected with saline excreted considerably less kallikrein than rats i.c.v. injected with d‐1‐propranolol (control saline: 162, s.e.m. = 14, n= 6; vs control d‐l‐propranolol: 559, s.e.m. = 20, n= 6). Even in stressed rats this difference was registered (stressed saline: 56, s.e.m. = 8, n= 6; vs stressed d‐l‐propranolol: 554 mAU per 100 g, s.e.m. = 33, n= 6).5. Peripheral sympathectomy with 6‐hydroxydopamine (6‐OHDA) did not suppress the hyperglycaemic response to stress, but it stimulated UKal. Kallikrein excretion was similar in 6‐OHDA stressed (534 mAU per 100 g, s.e.m. = 30, n= 6) than in 6‐OHDA control rats (491 mAU per 100 g, s.e.m. = 34, n= 6). No differences were observed on UNa and GFR between control 6‐OHDA treated rats and stressed 6‐OHDA treated rats.6. The present results suggest strongly that urinary kallikrein excretion is modulated by sympathetic activity. Results after central β‐adrenergic blockade and peripheral sympathectomy led to the hypothesis that normal sympathetic tone in the kidney inhibits the release of kallikrein into the urine.
GASTRIC MUCOSAL DEFENCE MECHANISM DURING STRESS OF PYLORIC OBSTRUCTION IN ALBINO RATS
Authors: Somasundaram K. , Ganguly A. K. 
Published: June 2007

SUMMARY1. The integrity of the gastric mucosa and its ability to secrete mucus are believed to be essential for protection of gastric mucosa against ulceration induced by aggressive factors active in any stress situation. This study involves a three‐compartmental analysis of gastric mucosal barrier in pylorus‐ligated albino rats.2. Quantitative analyses of histologically identifiable gastric mucosal epithelial neutral glycoproteins and gastric adherent mucus from oxyntic and pyloric gland areas, and components of non‐dialysable mucosubstances in gastric secretion were made under stress of pyloric obstruction for 4, 8, and 16 h durations. Epithelial mucin was identified by periodic acid‐Schiff (PAS) staining technique and assessed from the ratio of gastric mucosal thickness to the depth of PAS positive materials in it. The remaining visible mucus adhered to the gastric mucosa was estimated by Alcian blue binding technique. The results were compared with that of identical control groups.3. A significant reduction in mucosal epithelial PAS positive materials after 8 or 16 h of pylorus ligation was observed.4. The Alcian blue binding capacity of the pyloric gland area was increased significantly after 4 h of pylorus ligation, while after 8 or 16 h it was reduced in both oxyntic and pyloric gland areas.5. Significant reductions in the rate of gastric secretion and volume, as well as concentration of the components of non‐dialysable mucosubstances, were observed, indicating decreased synthesis of mucus glycoproteins.6. Disruption of the mucosal barrier may have occurred due to decreased mucus synthesis and acid‐pepsin accumulation; both could be due to stress associated with gastric distension.7. The present findings confirm the role of mucus in protecting the underlying gastric epithelium during stress. The adherent mucus offers a first line of defence and epithelial mucus a second line of defence.
DISSOCIATION BETWEEN CORTICOTROPHIN AND CATECHOLAMINE RESPONSES TO ISOPRENALINE IN HUMANS
Authors: Eisenhofer G. , Goldstein D. S. , Stull R. W. , Gold P. W. , Keiser H. R. , Kopin I. J. 
Published: June 2007

SUMMARY1. The pituitary‐adrenocortical, sympathoadrenomedullary and renin‐angiotensin‐aldosterone systems contribute to circulatory and metabolic homeostasis during stress. One possible site of co‐ordination of these systems is the β‐adrenoceptor.2. To determine whether circulating β‐adrenoceptor agonists can act hormonally to stimulate these systems simultaneously, plasma concentrations of corticotrophin (ACTH), noradrenaline, adrenaline and plasma renin activity were measured during graded intravenous infusions of isoprenaline in 20 people.3. Administration of isoprenaline caused dose‐related increases in noradrenaline (94% at the highest dose) and renin activity (189%), but decreases in ACTH (25%) and adrenaline (20%), findings inconsistent with simultaneous activation of these systems by circulating β‐adrenoceptor agonists.
HUMAN VASCULAR α‐ADRENOCEPTORS: THE RELEVANCE OF SUBTYPES
Authors: Moulds R. F. W. , Stevens M. J. , Jenkin R. A. 
Published: June 2007

SUMMARY1. The post‐receptor mechanisms of α1 and α2‐adrenoceptor subtypes in guinea‐pig aorta and human digital arteries have been explored.2. Nifedipine antagonized contractile responses of human digital arteries to TL99 and methoxamine to a similar degree, thus suggesting that neither the α1 nor the α2 receptor is preferentially linked to calcium entry through voltage‐operated channels of the cell membrane.3. In the guinea‐pig aorta, which contains only α1‐adrenoceptors, methoxamine‐stimulated inositol phosphate (IP) production at similar concentrations was required to produce contractile responses.4. In the human digital artery, noradrenaline also produced a significant increase in IP formation, but preliminary experiments have suggested that both TL99 and methoxamine stimulate IP production.5. Thus, the present authors have been unable as yet to confirm, in a tissue which contains both α1‐and α2‐adrenoceptors, that the post‐receptor mechanisms of the α subtypes are different.
TIME DEPENDENT CONVERSION FROM α1‐ to β‐ADRENOCEPTOR‐ MEDIATED GLYCOGENOLYSIS IN ISOLATED RAT HEPATOCYTES: ROLE OF MEMBRANE PHOSPHOLIPASE A2 AND PROTEIN KINASE C
Authors: Ishac E. J. N. , Kunos G. 
Published: June 2007

SUMMARY1. Incubation of isolated rat liver cells in a serum‐free buffer leads to the reduction of the glycogenolytic effect of phenylephrine and the simultaneous emergence of the response to isoprenaline within 4 h.2. Inhibitors of phospholipase A2 reverse the adrenergic activation of phosphorylase a from a β‐ to an α1‐receptor‐mediated event. Conversely activators of phospholipase A2 enhance the conversion.3. In vitro incubation of hepatocytes leads to a translocation of protein kinase C from the cytosol to the membrane which can be mimicked by phorbol 12‐myristate 13‐acetate (PMA), an activator of protein kinase C. PMA is also associated with transformation from α1 to β‐adrenoceptor‐mediated glycogenolysis.4. It is proposed that coupling of hepatic α1 and β‐adrenoceptors to postreceptor pathways are regulated by changes in membrane phospholipase A2 and protein kinase C activity.
NATURE OF THE GASTRIC ACID‐GASTRIN FEEDBACK LOOP IN THE FETAL SHEEP
Authors: Shulkes Arthur , Chick Patricia , Hardy Kenneth J. 
Published: June 2007

SUMMARY1. The neonates of sheep and other species have a decreased gastric acid secretion but an elevated plasma gastrin concentration.2. Since low gastric acid secretion is a stimulus for gastrin release in mature animals the present study examined whether the relative hypochlorhydria in the sheep fetus was sustaining the hypergastrinaemia.3. Fetal plasma gastrin was measured following fetal gastric acidification (pentagastrin infusion) and gastric neutralization (parietal cell blockade with the proton pump inhibitor omeprazole) in chronically cannulated fetal sheep from 101 days until term (145 days).4. Acutely raising gastric pH with omeprazole increased plasma gastrin in the mature sheep. However, in the fetus increasing the pH with omeprazole or decreasing pH with pentagastrin had no effect on fetal plasma gastrin. This was true for fetuses from all age groups.5. The results indicate that the gastric acid‐gastrin feedback loop is not functional in the fetus and that the hypergastrinaemia at birth is therefore not the result of the relative hypochlorhydria.6. The time after birth when the gastric acid‐gastrin feedback loop matures remains to be determined.
HAEMODYNAMIC AND RENAL EFFECTS OF A NOVEL PROSTAGLANDIN ANALOGUE (L644, 122 (+ISOMER)) IN SHEEP
Authors: Tresham Janette J. , Whitworth Judith A. , Scoggins Bruce A. 
Published: June 2007

SUMMARY1. Merino‐cross ewes were given an intravenous injection of a prostaglandin analogue, (+)‐4‐{3‐[3‐[2‐(1 ‐hydroxycyclohexyl)ethyl]‐4‐oxo‐2‐thiazolidinyl]‐propyl} benzoic acid, at doses of 0.01,0.05 and 0.10 mg/kg, on separate days, to determine renal and haemodynamic responses.2. Peripheral vasodilatory effects, indicated by increases in heart rate and cardiac output, and falls in total peripheral resistance, peaked at 20 min at the two highest doses. By 60 min most values had returned to pre‐injection levels. There were no changes in mean arterial pressure.3. At the highest dose of 0.10 mg/kg there was a fall in glomerular filtration rate, renal blood flow and effective renal plasma flow within 20 min. Urinary sodium and potassium excretion also fell with all three doses tested.4. Plasma renin concentration increased at the 0.05 and 0.10 mg/kg doses and was still elevated at 60 min.5. The results of this study in the sheep contrast with others in the dog, where renal blood flow is increased and the rat, where blood pressure is increased, and indicate a species specificity in regard to the analogue's actions.
THE PATTERN OF ATRIAL NATRIURETIC PEPTIDE RELEASE DURING VENTRICULAR TACHYCARDIA IN MAN
Authors: Crozier Ian G. , Ikram Hamid , Nicholls M. Gary 
Published: June 2007

SUMMARY1. Plasma levels of atrial natriuretic peptide (ANP) are high in many patients with tachycardia, but patterns of release with onset and termination of tachycardia and relationships to haemodynamic recordings are not clear. Blood for ANP measurements was therefore drawn from the coronary sinus, femoral artery and femoral vein, and simultaneous haemodynamic recordings were made in five patients before, during and after induction of stable ventricular tachycardia for 30 min.2. Tachycardia induced increases in ANP to peak levels, 2.6 to 5.7 times higher than baseline values at 20 min or later, whereas maximum haemodynamic changes, including a rise in pulmonary artery diastolic pressure, were achieved within 4 min.3. Reversion to sinus rhythm resulted in immediate changes in haemodynamic recordings, whereas ANP levels in arterial and venous plasma fell sluggishly with an apparent half‐life of 9.6 and 7 min, respectively.4. The results support a central role for atrial pressure in determining ANP secretion, but demonstrate a temporal delay between changes in atrial pressure and ANP secretion.
VENOCONSTRICTION CAUSES DIFFERENT EFFECTS IN THE HINDQUARTERS VENOUS COMPARTMENT OF CATS AND DOGS*
Authors: Widdop R. E. , Bentley G. A. , Reynoldson J. A. , Cullen L. K. 
Published: June 2007

SUMMARY1. A study was made of venoconstrictor mechanisms in the hindquarters region of cats and dogs by the use of autoperfused hindquarter preparations, together with the measurement of vena cava blood flow (VCBF).2. Noradrenaline, adrenaline and angiotensin II (AII) were all administered intraarterially and their ability to alter perfusion pressure and VCBF was examined.3. All three drugs increased perfusion pressure in both cats and dogs as a result of increases in arterial resistance. At the same time, noradrenaline and adrenaline increased VCBF in cats, while AII had a variable effect. In contrast, all three drugs decreased VCBF in dogs.4. These differences in the venoconstrictor responses obtained in cats and dogs may be explained by an action of the drugs at different loci within the venous compartment of the two species.