bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of Hypertension in Renal Disease
Authors: Brod J. , Bahlmann J. , Cachovan M. , Pretschner P. 
Published: August 2015

1. Central and peripheral haemodynamics, circulating blood volume and plasma renin activity (PRA) were investigated under resting conditions in 97 patients with chronic nonuraemic renal parenchymatous disease and without anaemia. For comparison a group of 17 healthy subjects was used.
2. An initial abnormality appeared in 12 out of 32 normotensive renal patients. It consisted of a markedly increased circulating blood volume, raised cardiac output, low total peripheral and forearm vascular resistance, hyperfusion of the forearm and increased venous distensibility. PRA was slightly (but insignificantly) higher in these hyperkinetic subjects with relaxed peripheral vessels than in the other 20 normotensive renal patients who did not differ haemodynamically from the control subjects.
3. Fifteen out of 47 renal patients with a mild or moderate hypertension (stage I–II WHO) were hyperkinetic. However, in these there was no compensatory vasodilatation in response to the high cardiac output: forearm blood flow was normal and venous distensibility below that of the control subjects. Blood volume was normal. Plasma renin activity (PRA) was the same as in the normotensive renal patients.
4. The difference between stage I–II and stage III was due entirely to a rise in total peripheral vascular resistance.
5. A re-examination of these patients 2-8 years after they had been first studied revealed that 11 out of the 12 originally hyperkinetic normotensive renal patients were now hypertensive compared with only one-half of the originally normokinetic normotensive renal subjects.
6. It is concluded that an inability of the diseased kidney to control volume homoeostasis leads to hypervolaemia, which raises cardiac output in the renal patients whilst still normotensive. As long as the arterioles adjust to the high output and the capacitance system to the high volume, blood pressure remains normal. When this adaptation of the periphery ceases, blood pressure rises, normalizing (possibly through a pressure diuresis) blood volume. PRA does not correlate with any of these changes and only in advanced renal hypertension may its rise partly contribute to the maintenance of high blood pressure without being its cause.
Nocturnal Hypoxaemia in Chronic Obstructive Pulmonary Disease
Authors: Stradling J. R. , Lane D. J. 
Published: August 2015

1. Day and night arterial oxygen saturation (Sao2) has been measured in forty-one patients with chronic obstructive pulmonary disease (COPD), mean FEV1 0.84 (range 0.4-1.4) litres, and with a range of daytime Sao2 values of 67-95%.
2. The mean and biggest falls in Sao2 at night were much greater in the patients with lower daytime saturations. However, when falls in arterial oxygen tension (Pao2) were estimated from the decreases in Sao2, there was no correlation between the estimated biggest fall in Pao2 and daytime Sao2 and only a weak correlation between estimated mean fall in Pao2 and daytime Sao2.
3. Measurement of ventilation in four hypoxaemic patients with COPD (range 60-90% Sao2) by respiratory inductance plethysmography showed that nocturnal hypoxaemic dips were accompanied by diminished ventilation, which was not always shown by nasal thermistors.
4. Because nocturnal hypoxaemic dips are transient the ideal alveolar-arterial oxygen difference, which assumes a constant respiratory exchange ratio, cannot be used to assess the mechanism of hypoxaemia.
5. Erythrocyte mass was strongly correlated with daytime Sao2 but this correlation was not significantly improved by including nocturnal hypoxaemia in the regression.
6. The results suggest that greater falls in Sao2 at night are related to lower initial Sao2 values and that the cause-5-be a reduction in ventilation.
Adenosine Diphosphate-Degrading Activity in Placenta
Authors: Barradas M. , Khokher M. , Hutton R. , Craft I. L. , Dandona P. 
Published: August 2015

1. The degradation of ADP by the placenta and umbilical artery was investigated.
2. Supernatants from incubations of finely chopped placental and umbilical arterial tissue were incubated with [14C]ADP for various durations from 0 to 30 min.
3. Products of ADP degradation were separated by thin-layer chromatography and radioactivity incorporated into each product was measured.
4. Placental supernatants induced a more rapid degradation of ADP than the umbilical artery supernatants. The main product of ADP degradation by placental supernatants at 30 min was adenosine, whereas that of umbilical artery was AMP.
5. This conversion by placenta of ADP, a potent platelet aggregator and vasoconstrictor, into adenosine, a potent platelet anti-aggregator and vasodilator,-5-be important in the maintenance of perfusion of the foetoplacental unit.
The Epidemiology of Plasma Renin
Authors: Meade T. W. , Imeson J. D. , Gordon D. , Peart W. S. 
Published: August 2015

1. The epidemiological characteristics of plasma renin activity (PRA) were established in 1999 members of occupational groups in North and West London.
2. The main finding was that PRA was inversely associated with systolic blood pressure in men, the percentage fall in PRA (on a log scale) being 8.4% for each increase of one standard deviation in systolic blood pressure. There was a less obvious inverse relationship in women.
3. However, blood pressure accounted for less than 1% of the variance in PRA.
4. Mean PRA in both smokers and ex-smokers was about 20% higher than in non-smokers.
5. PRA fell with increasing age, was lower in women than in men and considerably lower in blacks (of either sex) than whites.
6. PRA was lower in the first quarter of the menstrual cycle than in the rest of the cycle.
7. Haemoglobin, blood cholesterol, leucocyte count and Factor VIII were positively correlated with PRA.
8. PRA was lower in men with diagnosed hypertension than in those without; there was no significant difference in the women.
9. PRA was lower in those who had had myocardial infarcts in the past than in those who had not.
10. The data as a whole suggest that it may be low, not high, levels of PRA which are associated with increased risks of cardiovascular disease in which hypertension is a predisposing factor.
11. The explanation may be a homoeostatic fall in PRA in response to a rise in blood pressure rather than a major causal role for PRA in the pathogenesis of essential hypertension and target-organ damage.
Purine Transport and Metabolism in Man: The Effect of Exercise on Concentrations of Purine Bases, Nucleosides and Nucleotides in Plasma, Urine, Leucocytes and Erythrocytes
Authors: Harkness R. A. , Simmonds R. J. , Coade S. B. 
Published: August 2015

1. After decreasing muscle ATP by a 2 min period of intense exercise, we have studied purine metabolism by using high-pressure liquid chromatography.
2. A major increase in hypoxanthine concentration in plasma and urine was found with increases in xanthine and, in plasma, inosine. Erythrocyte hypoxanthine rose with the level in plasma, but there was no corresponding rise in IMP, the first intracellular metabolite of hypoxanthine. No rises in uridine or urate were found in plasma.
3. Plasma adenosine did not rise and fall significantly after exercise, but a small rise and fall in adenine nucleotide concentrations in plasma was found.
4. Running, swimming and games, which tended to be at the weekend, were associated with a rise in hypoxanthine and xanthine excretion; exercise was probably the cause of the higher excretion during the day than at night. Such activities do not produce changes in concentrations of ATP in muscle, although turnover must rise.
5. The results are consistent with widespread purine exchange between tissues and a ‘circulating hypoxanthine pool’.
Mucosal Enzyme Activities, with Special Reference to Enzymes Implicated in Bicarbonate Secretion, in the Duodenum of Rats with Cysteamine-Induced Ulcers
Authors: Stiel Danny , Murray Denver J. , Peters Timothy J. 
Published: August 2015

1. Duodenal mucosa was collected from control rats and from animals which had received cysteamine, cysteamine plus cimetidine or pentagastrin. Animals which received cysteamine with or without cimetidine developed acute duodenal ulcers. Cysteamine treatment resulted in gastric acid hypersecretion, which was largely abolished by concurrent cimetidine administration.
2. Activities of enzymes implicated in bicarbonate secretion, HCO−3-activated ATPase, carbonic anhydrase and Na+ + K+-activated ATPase, were measured in the duodenal mucosa of control rats and animals 24 h after subcutaneous administration of cysteamine. Assays of these enzymes in duodenal mucosal homogenates from animals with cysteamine-induced ulcers showed significant decreases in HCO−3-activated ATPase and carbonic anhydrase activities compared with controls.
3. Alkaline phosphatase activity also fell significantly in the cysteamine-treated animals, and possibly reflects the HCO−3-activated ATPase activity in the brush-border membrane. in contrast, activities of other marker enzymes from the brush-border membrane and from several intracellular organelles were unchanged, indicating an absence of gross organelle pathology in this experimental model.
4. Similar changes in enzyme activity were not caused by treatment with pentagastrin. Administration of cimetidine with the cysteamine did not protect the animals against ulceration, and the activity of HCO−3-activated ATPase was persistently decreased. However, the carbonic anhydrase activity was unaltered in this latter group, compared with controls.
5. These findings suggest that in cysteamine-induced duodenal ulceration both gastric acid hypersecretion and impaired duodenal resistance occurs. It is suggested that decreased activities of key enzymes implicated in HCO−3 secretion may reflect the biochemical basis for the decreased mucosal resistance.
The Influence of a High Dietary Intake of Purine-Rich Animal Protein on Urinary Urate Excretion and Supersaturation in Renal Stone Disease
Authors: Fellström B. , Danielson B. G. , Karlström B. , Lithell H. , Ljunghall S. , Vessby B. 
Published: August 2015

1. Eight recurrent renal stone-forming patients were housed in a metabolic ward and fed on a low (LPD) and a high (HPD) animal protein diet, which were isoenergetic. Metabolic studies were made after 2 weeks on each diet.
2. There was a 90% increase in urinary urate on HPD compared with LPD, whereas serum urate did not change consistently.
3. The urinary acid excretion increased by 200%, including a 100% increase in ammonium ion excretion. A fall in urine pH by 0.9 unit was also seen.
4. The calculated ion activities of the urines revealed a profound increase in the uric acid supersaturation, from undersaturation to supersaturation, and in some cases even surpassing the formation product ratio. The ammonium urate supersaturation also increased. The sodium urate supersaturation was unchanged, despite an induced natriuresis.
5. The risk of forming uric acid or ammonium urate crystals or stones in the urine was increased on a high protein diet, whereas the risk of forming sodium urate crystals was no greater than on a low protein diet.
6. As uric acid and ammonium urate crystals under certain conditions may adsorb a macromolecular fraction of the human urine, which inhibits calcium oxalate crystal growth, it is proposed that this mechanism, along with a decrease in urine pH, may also interfere with the inhibitory activity of calcium oxalate crystal growth and aggregation.
Changes in the Number and Activity of Sodium Pumps in Erythrocytes from Patients with Hyperthyroidism
Authors: Rubython E. Jill , Cumberbatch M. , Morgan D. B. 
Published: August 2015

1. The sodium content, the rate and rate constant of ouabain-sensitive sodium efflux and the number of sodium pumps (indicated by the ouabain-binding capacity) were measured in erythrocytes from patients with hyperthyroidism and compared with values obtained in euthyroid patients and healthy control subjects. Erythrocyte zinc content was measured as a simple estimate of the content of carbonic anhydrase.
2. In the hyperthyroid patients, erythrocyte sodium content was increased, whereas the rate and rate constant of ouabain-sensitive sodium efflux, the ouabain-binding capacity and erythrocyte zinc content were all decreased.
3. The sodium pumps in hyperthyroidism had the same affinity for ouabain and the same rate constant per pump as those in healthy controls.
4. The decrease in the efflux rate constant could be entirely accounted for by the decrease in the number of sodium pumps.
5. Although the sodium efflux was decreased in the hyperthyroid patients, the change was less than expected for the decrease in the efflux rate constant. This suggests that there is an increase in the ground permeability of the erythrocyte membrane in hyperthyroidism.
6. In the hyperthyroid patients the number of sodium pumps and erythrocyte zinc content were inversely related to the plasma levels of thyroxine and tri-iodothyronine, but more closely to the latter.
7. These results suggest that the thyroid hormones may influence the erythrocyte's content of a range of proteins which happens to include the sodium pump.
α1-Antitrypsin and Reactive Systemic Amyloidosis
Authors: Maury C. P. J. , Teppo A.M. , Fröseth B. , Wegelius O. 
Published: August 2015

1. Serum contains amyloid A-degrading activity. This activity is markedly reduced in patients with rheumatoid arthritis (RA) complicated by amyloidosis. α1-Antitrypsin inhibits the degradative activity. To test the hypothesis that the activity of this enzyme is regulated by α1-antitrypsin, we determined the concentrations, elastase-inhibitory activity and phenotypes of α1-antitrypsin in 24 RA patients with and in 26 RA patients without amyloidosis.
2. α1-Antitrypsin concentrations and biological activity were significantly increased in both patient groups compared with control subjects, but there was no difference between the two patient groups.
3. All patients who had developed amyloidosis were of the normal protease inhibitor (Pi) MM-phenotype.
4. We conclude that the difference in the amyloid A-degrading activity between RA patients with or without amyloidosis cannot be accounted for by differences in concentration, activity or Pi type of α1-antitrypsin.
Effects of Ingested Steak and Infused Leucine on Forelimb Metabolism in Man and the Fate of the Carbon Skeletons and Amino Groups of Branched-Chain Amino Acids
Authors: Elia Marinos , Livesey Geoffrey 
Published: August 2015

1. The effects of ingested grilled beef steak (250 g raw weight of lean meat) and infusion of leucine (3.8 g) on human forelimb metabolism were studied by monitoring the concentrations of various metabolites in arterial (A) and venous (V) blood of four overnight fasted and rested men.
2. The mean basal A—V for branched-chain 2-oxo acid (BCOA) was small (−3.6 μmol/l). After ingestion of steak or administration of leucine there were large positive increases in the A—V for branched-chain amino acid (BCAA) but increase in the negative A—V for BCOA was relatively small.
3. Within 2 h of ingestion of steak, BCAA accounted for approx. 50% of those amino acids with a positive A—V and glutamine for up to 75% of those with a negative A—V; the negative A—V for alanine decreased to 10% of its basal value. Infusion of leucine produced a large positive A—V for leucine by forelimb, a doubling in the negative A—V for glutamine and a rise in the blood glutamine concentration; the negative A—V for alanine was virtually unchanged and the blood alanine concentration showed a late significant decrease.
4. After ingestion of steak there was a two- to three-fold rise in the arterial insulin concentration, little change in the positive A—V for glucose and a decreased negative A—V for ‘glycolytic products’ (alanine + lactate + pyruvate), suggesting increased utilization of glucose carbon. Infusion of leucine doubled the arterial insulin concentration; the A—V for glucose decreased, that for lactate, pyruvate and alanine remained unchanged, suggesting decreased utilization of glucose carbon.
5. Circulating BCOA was distributed almost entirely in the plasma space.
6. in a variety of clinical conditions (insulin-dependent diabetes, cirrhosis, muscular dystrophy and starvation), the basal plasma concentrations of BCOA correlated well with those of BCAA (r = 0.989). Infusion of leucine increased the plasma BCAA/BCOA ratio to the same extent (about 40%) in each clinical condition despite considerable variations in the rate of leucine clearance.
7. The observations indicate that both ingested steak and infused leucine produce important changes in the selection of respiratory fuels by the human forelimb, that BCOA is preferentially oxidized rather than released from human limb tissues, and that glutamine, not alanine, is the major amino group carrier leaving the forelimb both after a protein meal and after leucine administration. Changes in cellular uptake or transamination of leucine appear not to be responsible for the varied rates of leucine clearance in a variety of clinical conditions.
Aminophylline and Fatigue of Adductor Pollicis in Man
Authors: Wiles C. M. , Moxham J. , Newham D. , Edwards R. H. T. 
Published: August 2015

1. The effect of intravenous aminophylline on the contractility of adductor pollicis has been studied in three subjects both in the fresh state and following the induction of muscle fatigue.
2. Aminophylline had no influence on the frequency—force relationship and relaxation rate of adductor pollicis in the fresh state.
3. Fatigue resulted in a selective depression of the force response to low and moderate frequencies of stimulation and a slight effect on maximum force production 10 and 35 min afterwards.
4. Aminophylline given prior to, during and/or after fatigue did not influence this selective low-frequency fatigue at 10 or 35 min.
5. Aminophylline at the concentrations obtained has no significant effect on muscle contractility or fatiguability in man.
Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats
Authors: Handa Michiko , Kondo Kazuoki , Suzuki Hiromichi , Saruta Takao 
Published: August 2015

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment.
2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented.
3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.
Abnormalities of Calcium Metabolism in Essential Hypertension
Authors: Strazzullo P. , Nunziata V. , Cirillo M. , Giannattasio R. , Ferrara L. A. , Mattioli P. L. , Mancini M. 
Published: August 2015

1. Calcium metabolism has been investigated in patients with essential hypertension and normal renal function to evaluate the renal calcium handling and the reported increase in renal calcium loss.
2. In 55 hypertensive and 55 sex- and age-matched healthy normotensive subjects creatinine clearance, serum total and ionized calcium, plasma parathyroid hormone and 24 h urinary excretion of calcium, sodium and cAMP were measured. In a subgroup of 20 hypertensive patients and 20 controls the fasting calcium excretion rate was also measured.
3. Both 24 h and fasting calcium excretion rates were higher in the hypertensive group; so also were plasma parathyroid hormone and urinary cAMP. Serum total and ionized calcium levels were not different in the two groups.
4. After intravenous calcium infusion (15 mg 3 h−1 kg−1) in seven hypertensive patients and controls, the hypertensive patients excreted more calcium at all serum calcium concentrations.
5. These results support the hypothesis of primary renal calcium leak in essential hypertension. Enhanced urinary calcium excretion rate may cause compensatory parathyroid overactivity.
The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man
Authors: Struthers A. D. , Reid J. L. , Whitesmith R. , Rodger J. C. 
Published: August 2015

1. Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the β-adrenoceptor antagonists, atenolol or timolol.
2. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (− 8 beats/min).
3. Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 ± 0.02 s to 0.41 ± 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol.
4. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a β2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.
Effects of Indomethacin on the Guinea-Pig Pulmonary Response to Intravenous Leukotrienes C4 and D4
Authors: Leitch A. G. , Austen K. F. , Corey E. J. , Drazen J. M. 
Published: August 2015

1. We measured pulmonary conductance (GL), dynamic compliance (Cdyn.), and arterial pressure in chloralose-urethane anaesthetized guinea pigs for 30 min after intravenous infusion of either leukotriene (LT) C4 (1 μg/kg) or LTD4(0.5 μg/kg) to control or indomethacin-pretreated (30 mg/kg) animals.
2. LT infusion to control animals caused decrements in GL, which were maximal at 30 s and persisted for 7.5 min (LTD4) and 15 min (LTC4), decrements in Cdyn., which were maximal at 30 s and persisted for 30 min, and hypotension.
3. Indomethacin treatment before LT infusion significantly altered the changes in GL by reducing the early (&lt; 1 min) response and potentiating the later (3-5 min) response, significantly reduced the fall in Cdyn. at all time points, resulting in a change in the GL/Cdyn. ratio to 1.0 and prolonged the hypotensive response.
4. We conclude that cyclo-oxygenase products are responsible for the early (&lt; 1 min) pulmonary response to LT infusion and modulate the later (3-5 min) response but do not cause hypotension. With cyclo-oxygenase inhibition, the significant. primary activity of LT is possibly less preferentially directed to contractile tissues associated with small airways.