bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of the Malate-Aspartate Shuttle in Renal Sodium Transport in the Rat
Authors: Ross B. , Silva Patricio , Bullock Sarah 
Published: August 2015

1. Experiments were designed to establish the relationship between renal gluconeogenesis and sodium transport. Six inhibitors of gluconeogenesis, with different sites of action, were tested in the isolated perfused rat kidney in which renal function, and in particular Na+ reabsorption, was followed.
2. In kidneys from fed or starved rats specific inhibitors of gluconeogenesis neither inhibited nor stimulated Na+ reabsorption; gluconeogenesis and sodium reabsorption are therefore independent of one another under these conditions.
3. Inhibitors of transaminase or malic dehydrogenase inhibited gluconeogenesis from lactate and pyruvate respectively; the transaminase inhibitor significantly inhibited oxidation of lactate and glucose.
4. Sodium reabsorption was inhibited by a transaminase inhibitor when glucose or lactate was the sole substrate, and by inhibition of malic dehydrogenase when pyruvate was the substrate.
5. These results indicate that the malate-aspartate shuttle controls Na+ reabsorption in the intact kidney by regulating substrate oxidation (and the provision of energy) rather than by any direct involvement of gluconeogenesis in Na+ transport.
Effects of Methandienone on the Performance and Body Composition of Men Undergoing Athletic Training
Authors: Hervey G. R. , Knibbs A. V. , Burkinshaw L. , Morgan D. B. , Jones P. R. M. , Chettle D. R. , Vartsky D. 
Published: August 2015

1. In a previous study of the effects of methandienone (Dianabol) on men undergoing athletic training, strength and performance increased, but not significantly more when the subjects were taking the drug than when they were taking placebo. The subjects did, however, gain more weight on the drug, with increases in total body potassium and muscle dimensions. It remained an open question whether the muscles had gained normal tissue or intracellular fluid.
2. In an attempt to distinguish between these possibilities the trial has been repeated, using as subjects seven male weight-lifters in regular training, and including measurements of total body nitrogen. As before, a dose of 100 mg of methandienone/day was given alternately with the placebo in a double-blind crossover experiment. The treatment periods lasted 6 weeks and were separated by an interval of 6 weeks. Body weight, potassium and nitrogen, muscle size, and leg performance and strength increased significantly during training on the drug, but not during the placebo period.
3. The finding of increased body nitrogen suggested that the weight gain was not only intracellular fluid. The increases in body potassium (436 ± sem 41 mmol) and nitrogen (255 ± 69 g) were too large in proportion to the weight gain (2.3 ± 0.4 kg) for this to be attributed to gain of normal muscle or other lean tissue, and imply gain of nitrogen-rich, phosphate-poor substance. Although this action of methandienone might be described as anabolic, the weight gain produced is not normal muscle.
Effect of Magnesium Deficiency and Excess on Renal Tubular Potassium Transport in the Rat
Authors: Carney S. L. , Wong N. L. M. , Dirks J. H. 
Published: August 2015

1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling.
2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion.
3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.
Relations between Sodium Transport and Sodium Concentration in Human Erythrocytes in Health and Disease
Authors: Cumberbatch M. , Morgan D. B. 
Published: August 2015

1. We have examined the inter-relationships between erythrocyte sodium content and sodium transport in a group of healthy subjects and in groups of patients with disorders known to change the sodium content of erythrocytes.
2. In the healthy subjects the sodium content of erythrocytes was inversely related to both the permeability of the erythrocyte membrane to sodium (as measured by the unidirectional, ouabain-sensitive, sodium efflux) and the total activity of the sodium pumps (as measured by the rate constant of ouabain-sensitive sodium efflux). There was a correlation between the total activity of the sodium pumps and the membrane permeability to sodium.
3. Changes in the erythrocyte sodium content were due to a decrease in the activity of the sodium pumps (as in hypokalaemia and digoxin treatment), or a decrease in the permeability of the erythrocyte membrane to sodium (as in chronic renal failure) or a reduction of both the membrane permeability and the number of sodium pumps (as in hyperthyroidism or elderly patients).
4. One interpretation of the results in the healthy subjects is that there are two components of sodium influx; one associated with the sodium pumps in what we have called ‘membrane-units’ and the other determined by the ground permeability of the membrane.
5. On the basis of this model we suggest that in the geriatric and hyperthyroid patients there is a reduction in the number of ‘membrane-units’, that in hypokalaemia and during digoxin treatment there is inhibition of the sodium-pump component of the ‘membrane-units’ and that in chronic renal failure there is a decrease in the permeability of the membrane to sodium.
The Effect of Aging on β-Adrenoceptor-Stimulated Cyclic AMP Formation in Human Lymphocytes
Authors: Kraft C. A. , Castleden C. M. 
Published: August 2015

1. Responsiveness of the β-adrenoceptor adenylate cyclase system was measured in lymphocytes from healthy young and old subjects by incubating the cells with isoprenaline in the presence of a phosphodiesterase inhibitor and by measuring production of adenosine 3′:5′-cyclic monophosphate (cyclic AMP) with a competitive binding assay.
2. The two groups did not differ significantly in the levels of cyclic AMP produced or in the concentration of isoprenaline required to give half-maximal stimulation of the cells (ED50).
The Effects of Sustained Lung Inflation on the Pattern of Breathing in Man
Authors: Pearson S. B. , Heath J. R. 
Published: August 2015

1. Continuous positive-pressure breathing (CPPB) at airway pressures of 0.65–1.00 kPa above ambient pressure has been used to produce a sustained inflation of the lungs of approximately 1 litre in six normal male subjects.
2. Lung inflation produced a reduction in the ventilatory response to carbon dioxide inhalation by slow rebreathing in oxygen over approximately 45 min, with a reduction in the slope of the VE/Pet,CO2 and VT/Pet,CO2 relations (Pet,CO2, = end-tidal Pco2).
3. The pattern of breathing is altered, so that for any given expired minute ventilation (VE), tidal volume (VT) is reduced with a fall in breath duration (Tt) resulting from a decrease in inspiratory time (Ti) with no change in expiratory time (Te).
4. The break point on the VT/Ti relation is lowered.
Metabolism of Antithrombin III in Cirrhosis and Carcinoma of the Liver
Authors: Chan Vivian , Lai C. L. , Chan T. K. 
Published: August 2015

1. The metabolism of human antithrombin III (ATIII) was studied by using 125I-labelled tracer.
2. The plasma half-life (t0.5) was 2.71 ± 0.26 days in normal subjects and was similar in patients with cirrhosis or primary carcinoma of liver.
3. Patients with cirrhosis had low ATIII levels, decreased intravascular mass, total body mass and decreased absolute catabolic rate, suggesting decreased synthesis. The positive correlation of ATIII level with fractional catabolic rate (K10) indicated that the decreased catabolism might exert a positive inhibition on ATIII production.
4. These abnormalities were more exaggerated in patients with macronodular cirrhosis associated with hepatitis surface antigen or in those with ascites.
5. In cirrhotic patients with ascites an additional extravascular pool of ATIII was present which did not turn over at the same rate as the intravascular pool.
6. Patients with primary carcinoma of liver had moderately low ATIII, but normal intravascular mass and total body mass because of the increased plasma volume and normal absolute catabolic rate.
7. The negative correlation of ATIII levels with K10 suggested that the low levels could be due to increased catabolism or consumption.
8. One patient with disseminated malignancy and active superficial thrombophlebitis had normal ATIII metabolism.
Pubertal Induction of Sweat Gland Activity
Authors: Rees J. , Shuster S. 
Published: August 2015

1. To study the difference in sweat rate between men and women the rates of cholinergic-induced sweating were measured in normal people before and after puberty and in response to androgens and anti-androgens.
2. Sweat rate in men was more than double that in women.
3. This difference did not occur in prepubertal boys and girls in whom the rate, corrected for surface area, was comparable with that in women.
4. Application or injection of androgen locally did not stimulate sweat production in the adult female.
5. Anti-androgen topically or systemically did not decrease sweat rate in men.
6. It is concluded that the rate of sweat rate in men is caused by androgen-induced gene expression at puberty and not by androgen modulation in adult life.
Changes in Renal and Urinary Kallikrein Activity by Mannitol-Induced Osmotic Diuresis
Authors: Bönner G. , Marin-Grez M. , Beck D. , Deeg M. , Gross F. 
Published: August 2015

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol.
2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion.
3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance.
4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration.
5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.
The Effects of Meclofenamate, Captopril and Phentolamine on Organ Blood Flow in the Conscious Rabbit
Authors: Banks R. A. , Beilin L. J. 
Published: August 2015

1. Systemic and regional vascular changes were measured in conscious rabbits after intravenous sodium meclofenamate, captopril and phentolamine. These drugs were used respectively to inhibit prostaglandin synthesis and angiotensin-converting enzyme, and to block α-adrenoceptors.
2. Meclofenamate reduced renal and adrenal blood flow by 11 and 28% respectively, and doubled hepatic artery flow. The effect on renal and adrenal flow persisted in the presence of phentolamine.
3. Captopril decreased estimated peripheral resistance and increased cardiac output without changing arterial pressure. Kidney and adrenal flow increased by 70 and 21% respectively.
4. Phentolamine reduced arterial pressure and doubled flow to skeletal muscle and increased hepatic artery flow to the liver.
5. Splenic blood flow was unaffected by meclofenamate, captopril or phentolamine alone. Meclofenamate given after captopril caused a halving of splenic flow and a rise in arterial pressure; these effects were prevented by phentolamine.
6. The results point to a continuing effect of prostaglandin synthesis in maintaining blood flow to the kidney and adrenal gland independent of α-adrenoceptor activation in resting conscious rabbits. An important modulating effect of prostaglandins on sympathetic vascular tone in the spleen is suggested.
Changes in Vascular Ionic Composition at Different Stages of DOC-Salt Hypertension in the Rat
Authors: Villamil M. F. , Amorena C. , Ponce J. , Müller A. , Taquini A. C. 
Published: August 2015

1. Sequential changes in the ionic composition of the aorta and skeletal muscle were followed during 1, 2 and 4–6 weeks in 30 rats given deoxycorticosterone (DOC) and salt supplemented with potassium chloride. Twenty-one rats, drinking water, were used as controls.
2. Twenty-five per cent of the test rats were hypertensive after 1 week, 60% after 2 weeks and 100% after 4–6 weeks.
3. Muscle potassium fell in all test rats by an average of 15%. In contrast, aortic potassium fell by 19% only in those rats which did not develop hypertension after 1 week.
4. Total and non-inulin sodium and water of the aorta were normal in rats which remained normotensive after 1 or 2 weeks and high in those which became hypertensive during the same period.
5. Total sodium and water content of the aorta were also high in rats which were hypertensive at 4–6 weeks. However, because of simultaneous expansion of the inulin space, non-inulin fractions were normal in this group.
6. Results suggest that vascular ionic changes participate in the pathogenesis of DOC-salt hypertension through more than a single mechanism.
Venous Plasma Histamine in Exercise- and Hyperventilation Induced Asthma in Man
Authors: Barnes P. J. , Brown M. J. 
Published: August 2015

1. Venous plasma histamine was measured by a specific and sensitive radioenzymatic assay in seven male extrinsic asthmatic and six age-matched non-atopic non-asthmatic male subjects during exercise and voluntary isocapnic hyperventilation.
2. There was no change in peak expiratory flow in normal subjects with exercise or hyperventilation, but asthmatic subjects showed a 29.4 ± sem 5.8% fall after exercise and a 29.0 ± 5.4% fall after matched hyperventilation.
3. Plasma histamine was significantly higher (P &lt; 0.05) in asthmatic (6.2 ± 0.95 nmol/l) than that in normal subjects (3.4 ± 0.61 mmol/l) and showed a significant (P &lt; 0.01) rise (to 14.4 ± 1.83 nmol/l) during exercise in asthmatic, but not in normal subjects. This suggests that discharge of mast-cell mediators may occur during exercise in asthmatic subjects who develop exercise-induced asthma.
4. With hyperventilation there was no change in plasma histamine in either asthmatic or normal subjects, but this does not exclude the possibility that mediators may be released locally in the airways.
Role of the Brain Iso-Renin-Angiotensin System in Experimental Hypertension in Rats
Authors: Suzuki Hiromichi , Kondo Kazuoki , Handa Michiko , Saruta Takao 
Published: August 2015

1. To examine the possible participation of the brain iso-renin-angiotensin system in the control of blood pressure, as well as in the regulation of plasma renin activity, saralasin and captopril were injected into the cerebral ventricles of three types of experimental hypertensive rats with different plasma renin profiles.
2. Injection of saralasin and captopril into the cerebral ventricles resulted in a significant decrease in blood pressure of two-kidney, one-clip Goldblatt hypertensive rats (11 ± 2 and 9 ± 3 mmHg respectively) and that of spontaneously hypertensive rats (13 ± 2 and 12 ± 2 mmHg respectively), but in deoxycorticosterone (DOC)-salt hypertensive rats injection of these two agents showed a significant increase in blood pressure (13 ± 2 and 12 ± 3 mmHg respectively).
3. The plasma renin activity was markedly decreased after injection of saralasin and captopril into the cerebral ventricles of two-kidney, one-clip Goldblatt hypertensive rats. Conversely, in DOC-salt hypertensive rats, the plasma renin activity was markedly increased after injection of these two agents. In spontaneously hypertensive rats these agents caused no significant change in plasma renin activity.
4. These findings suggest that the brain iso-renin-angiotensin system participates in the central regulation of blood pressure and may be responsible for modulation of the peripheral renin-angiotensin system.
Inhibition of the Renin-Angiotensin-Aldosterone System by l-Dopa with and without Inhibition of Extracerebral Dopa Decarboxylase in Man
Authors: Barbieri C. , Caldara R. , Ferrari C. , Crossignani Rosa Maria , Recchia M. 
Published: August 2015

1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man.
2. Eight normal subjects received in a randomized order placebo, l-dopa (500 mg, orally) and l-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses).
3. l-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P &lt; 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P &lt; 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P &lt; 0.05 at 120 and 150 min, P &lt; 0.01 at 180 min) and in plasma aldosterone concentration (P &lt; 0.05 at 30 and 60 min, P &lt; 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens.
4. Since l-dopa, as well as l-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.
Dexamethasone, Aldosterone and Kallikrein Release by Isolated Rat Kidney
Authors: Vio C. P. , Roblero J. S. , Croxatto H. R. 
Published: August 2015

1. The effect of d-aldosterone and dexamethasone on kallikrein release was studied in the isolated rat kidney perfused with modified Krebs-Henseleit buffer.
2. Animals received d-aldosterone or dexamethasone (10 μg/100 g body weight) daily for 3 days. Their isolated kidneys were then perfused with the same steroids at rates of 2.0–2.5 μg/min for 30 min.
3. Dexamethasone increased kallikrein release significantly (P &lt; 0.001) both in urine and in venous outflow.
4. d-Aldosterone had no significant effect on kallikrein release, either in urine or in venous outflow.
Increased Hepatic Fibrogenesis in the Cholesterol-Fed Mouse
Authors: Lee S. P. 
Published: August 2015

1. Mice when fed a cholesterol/choline-supplemented diet for 4 weeks developed histologically fatty livers. This lipid overloading was associated with an increase in hepatic concentration of connective tissues.
2. Both histological and biochemical abnormalities regressed on stopping the cholesterol diet for another 4 weeks. With continuing feeding for 24 weeks these abnormalities were sustained.
3. In the absence of available evidence that cholesterol is ‘toxic’ to the liver, it is concluded that lipid loading alone increases hepatic fibrogenesis.
Effect on Blood Lipids and Haemostasis of a Supplement of Cod-Liver Oil, Rich in Eicosapentaenoic and Docosahexaenoic Acids, in Healthy Young Men
Authors: Sanders T. A. B. , Vickers Marguerite , Haines A. P. 
Published: August 2015

1. Twelve healthy male subjects took a daily supplement of 20 ml of cod-liver oil for 6 weeks. This provided 1.8 g of eicosapentaenoic acid (20:5ω3) and 2.2 g of docosahexaenoic acid (22:6ω3). The effects of the supplement on blood lipids, haemostatic variables, bleeding time and plasma vitamin A and carotene were studied. In seven subjects platelet aggregation induced by adenosine 5′-pyrophosphate (ADP) was also studied.
2. The proportions of 20:5ω3 and 22: 6ω3 in platelet and erythrocyte phosphoglycerides were substantially increased by the supplement mainly at the expense of ω6 polyunsaturated fatty acids.
3. Mean plasma triglyceride concentrations were reduced and those of high-density-lipoprotein (HDL) cholesterol were increased by the supplement.
4. The mean bleeding time was significantly prolonged after 3 weeks of taking the supplement, but had returned to the presupplementation value 5 weeks after withdrawal of the supplement.
5. The maximum estimated response to platelet aggregation induced by ADP was increased by the supplement.
6. The mean levels of antithrombin III (immunological) and blood pressure were lower at the end of the period of supplementation and remained so 5 weeks after withdrawal of the supplement. No significant changes in other variables were noted.
Cardiovascular Effects of Vasopressin Infused into the Vertebral Circulation of Conscious Dogs
Authors: Liard J. F. , Dériaz O. , Tschopp M. , Schoun J. 
Published: August 2015

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min−1 kg−1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured.
2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously.
3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.
Characterization of Aggression-Provoked Renin from An Unknown Source in Male Mice
Authors: Poulsen K. , Pedersen E. B. 
Published: August 2015

1. In male mice without kidneys and submaxillary, as well as sublingual, glands aggressive behaviour causes a vast release of renin [J. Bing & K. Poulsen (1979) Acta Physiologica Scandinavica, 107, 251–256].
2. This resulted in about an 800-fold increase in plasma renin concentration from the control level of 0.52 (range 0.15-0.8) Goldblatt unit (G.U.) × 10−3/ml to 430 (range 300–500) G.U. × 10−3/ml after aggression.
3. The aggression-provoked renin fulfil all the criteria so far studied for being active renin, identical with normal mouse plasma renin and pure submaxillary mouse renin.
4. It generates angiotensin I with renin substrate and Km (1.2 μmol/l) is the same. It is neutralized by pepstatin but not by inhibitors of metallo-, thiol and serine proteinases, indicating that it is an aspartate proteinase (acidic proteinase).
5. It is a 40 000-mol.wt. renin, which has full enzymatic activity with a specific enzymatic activity of 0.32 G.U./μg, identical with that of normal plasma renin.
6. Its enzymatic activity is neutralized by a specific antibody against pure submaxillary renin. It is measurable in the direct renin radioimmunoassay with a dilution curve which parallels that of the standards. It demonstrates complete antigenic identity with pure submaxillary renin in crossed immunoelectrophoresis.
7. Its origin is unknown.