bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alcohol: Effect on Blood Pressure and Predisposition to Hypertension
Authors: Arkwright P. D. , Beilin L. J. , Rouse I. , Armstrong B. K. , Vandongen R. 
Published: August 2015

1. The association between alcohol consumption and blood pressure was studied in 491 Government employees. The men, aged 21–45 years, volunteered to complete a health questionnaire and submitted to standardized measurements of blood pressure, heart rate and body size.
2. Average weekly alcohol consumption correlated with systolic pressure (r = 0.18, P &lt; 0.001) but not with diastolic pressure. Systolic pressure increased progressively with increasing alcohol consumption with no obvious threshold effect. The effect of alcohol was independent of age, obesity (Quetelet's index) or cigarette smoking.
3. Results indicate that alcohol ranks close to obesity as a preventable cause of essential hypertension in the community.
Accuracy of the London School of Hygiene and Remler M2000 sphygmomanometers
Authors: Fitzgerald D. J. , O'Callaghan W. G. , O'Malley K. , O'Brien E. T. 
Published: August 2015

1. The accuracy of the Remler M2000, a semiautomatic portable blood pressure recorder, was assessed with the London School of Hygiene (LSH) and Hawkesley random-zero sphygmomanometers used as reference standards.
2. The Remler gave higher recordings than the LSH sphygmomanometer, the mean systolic and diastolic differences being 5.9 mmHg (P &lt; 0.001) and 4.7 mmHg (P &lt; 0.001) respectively. No significant difference was demonstrated between paired Remler and Hawkesley recordings.
3. When simultaneous paired LSH and Hawkesley sphygmomanometer recordings were compared, the LSH gave lower blood pressures: 7.1 mmHg (P &lt; 0.001) for systolic and 3.6 mmHg (P &lt; 0.001) for diastolic recordings.
4. The LSH sphygmomanometer underestimates blood pressure, partly due to a calibration error but also because the selection of end points for this device differs from other methods of blood pressure measurement.
Haemodynamic Effects of Withdrawal of Long-Term Treatment with β-Adrenoceptor Blocking Agents in Subjects with Essential Hypertension
Authors: Bengtsson C. , Larsson Y. , Panfilov V. , Sivertsson R. , Åström H. 
Published: August 2015

1. After 10 years of β-adrenoceptor blockade in five female patients with essential hypertension, the β-adrenoceptor-blocking agent was withdrawn, and the women were then followed up for 1 year, with measurements of cardiac output and peripheral resistance.
2. Blood pressure remained low during the first year after withdrawal in spite of the fact that the heart rate increased within the first few days.
3. Cardiac output was found to increase during the first year after withdrawal, although total peripheral resistance was essentially unchanged.
4. The maintenance of low blood pressure after withdrawal of the antihypertensive drug might indicate a regression of structural changes in the resistance vessels during successful long-term antihypertensive treatment.
5. Minimal resistance in hands and calves did not increase during the year after withdrawal.
Effects of Short-Term and Long-Term Treatment with Cardio-Selective and non-Selective β-Receptor Blockade on Carbohydrate and Lipid Metabolism and on Plasma Catecholamines at Rest and during Exercise
Authors: Koch G. , Franz I.-W. , Lohmann F. W. 
Published: August 2015

1. The effects on glucose and lipid metabolism and on plasma catecholamines at rest and during exercise, of 4 weeks treatment with non-selective β-blockade (pindolol, 15 mg daily) and with cardio-selective blockade (metoprolol, 200 mg, and acebutolol, 500 mg, respectively) were compared in different groups of hypertensive men (mean age 37 years) by single blind cross-over technique. All patients continued the treatment with either metoprolol or acebutolol for another 12–14 months.
2. All antagonists reduced blood pressures and exercise heart rates in a virtually identical manner. Whereas lipolysis was similarly inhibited by both selective β1-antagonists and non-selective β1-β2-blockers, glycogenolysis in the muscle was inhibited only by non-selective β-receptor blockade.
3. The inhibition of glycogen breakdown resulted in exercise hypoglycaemia and in increases of plasma adrenaline and ACTH, which probably reflect counter-regulatory mechanisms. No major metabolic changes occurred after 12–14 months compared with 4 weeks of treatment.
Decrease in α-Adrenoceptor-Mediated Vasoconstriction Parallels the Antihypertensive Response to Propranolol in Patients with Normal Renin Essential Hypertension
Authors: Amann F. W. , Bolli P. , Hulthén L. , Kiowski W. , Bühler F. R. 
Published: August 2015

1. α1-Adrenoceptor-mediated vasoconstriction was studied before and during propranolol therapy in eight normal renin essential hypertensive patients; four were known ‘responders’ and four, age-matched ‘non-responders’ to previous β-receptor blocker monotherapy. Plasma renin activity, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during regional postjunctional α1-adrenoceptor blockade with prazosin. All measurements were done on placebo and again after 6 weeks’ propranolol monotherapy (320 mg/day).
2. Propranolol reduced heart rate and plasma renin activity to the same extent in ‘responders’ and ‘non-responders’. Resting plasma adrenaline concentrations tended to be higher in ‘responders’ before propranolol; they remained unchanged in both groups on propranolol. Plasma noradrenaline concentrations were similar in both groups before and on propranolol.
3. Before propranolol forearm flow was not different in ‘responders’ and ‘non-responders’. Non-specific vasodilatation with sodium nitroprusside produced a similar increase in forearm flow before and after propranolol in both groups.
4. Prazosin-induced increments in forearm flow tended to be higher in ‘responders’ before propranolol. After propranolol the vasodilator effect of prazosin was attenuated in ‘responders’ but it remained unchanged in ‘non-responders’ (P &lt; 0.01).
5. In patients with normal renin essential hypertension the antihypertensive response to propranolol monotherapy is paralleled by a decrease in postjunctional α1-adrenoceptor-mediated vasoconstriction.
Effects of Prizidilol (SKF 92657) on Blood Pressure, Haemodynamics, Sympathetic Nervous System Activity and Plasma Volume in Essential Hypertension
Authors: Fariello R. , Alicandri C. L. , Agabiti-Rosei E. , Romanelli G. , Castellano M. , Beschi Marina , Platto Letizia , Di Priolo Susanna Leto , Muiesan G. 
Published: August 2015

1. The antihypertensive effect of 4 weeks' treatment with prizidilol (SKF 92657) (mean dosage 520 mg once or twice daily) was studied in ten essential hypertensive patients.
2. Both systolic and diastolic blood pressure were significantly reduced in all cases. Supine heart rate did not change, and in the erect position heart rate was significantly lowered.
3. Blood pressure reduction was due to peripheral vasodilatation, as the cardiac index increased after 4 weeks of prizidilol treatment.
4. After prizidilol plasma noradrenaline and adrenaline increased significantly, and PRA and plasma aldosterone were reduced. Although plasma volume increased, body weight did not change.
5. Cardiac performance, as evaluated by the PEP/LVET ratio, improved after treatment with prizidilol.
Role of Prostaglandins in Mediating Excretion by the Kidney of an Intravenous Infusion of Sodium Chloride in Normal Human Subjects
Authors: Watson M. L. , Lambie A. T. , Thom A. , Ungar A. 
Published: August 2015

1. Normal male subjects were given a rapid infusion of 3 litres of sodium chloride solution (150 mmol/l) with or without pretreatment with indomethacin.
2. There was marked individual variability in the rate at which the infused sodium chloride solution was subsequently excreted which was not related to the urinary sodium excretion in the previous 24 h.
3. There was no relationship between urinary prostaglandin E excretion during the 24 h preceding the sodium chloride infusion and the rate at which different individuals subsequently excreted sodium and water.
4. Renal plasma flow was significantly higher during the sodium chloride infusion than in the post-infusion recovery period, both with and without pretreatment with indomethacin, although it was significantly lower during each period in subjects pretreated with indomethacin.
5. Urinary prostaglandin E excretion was significantly decreased after the infusion of sodium chloride solution.
6. Indomethacin slightly decreased the rate of excretion of sodium and water.
7. Prostaglandins have a role in, but are not the main determinants of, the excretion of an intravenous infusion of sodium chloride.
8. The results do not support the suggestion that prostaglandin E produced within the kidney, as indicated by urinary prostaglandin E excretion, exerts a natriuretic action.
Pathogenesis of Salt Retention in Dogs with Chronic Bile-Duct Ligation
Authors: Chaimovitz C. , Alon U. , Better O. S. 
Published: August 2015

1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL).
2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 ± 62 vs 960 ± 58 μmol/min in the control period before CBDL (P &lt; 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 ± 5.5 pg/ml before CBDL to 177 ± 50 pg/ml after CBDL (P &lt; 0.02). Ascites was present in all salt-retaining CBDL dogs.
3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 ± 124 μmol/min, a value significantly higher than in the CBDL dogs with intact adrenals (P &lt; 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies.
4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) an extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.
Intracellular Free Amino Acids in Undernourished Patients with or without Sepsis
Authors: Milewski P. J. , Threlfall C. J. , Heath D. F. , Holbrook I. B. , Wilford K. , Irving M. H. 
Published: August 2015

1. Thigh muscle samples for analysis were obtained from 35 control subjects and 12 severely ill patients, of whom five had disease-induced undernutrition and seven had associated sepsis. An improvement in the Bergström technique for analysing muscle needle biopsy samples was used.
2. Muscle water, chloride and DNA were increased in both groups of ill patients, indicating an increase in the extracellular component and loss of muscle protein.
3. Falls in the concentrations of glutamine, glutamate, arginine, histidine, ornithine and lysine and rises in those of glycine, serine, asparagine, tyrosine, valine, leucine, isoleucine, phenylalanine, methionine and tryptophan were observed in the group of ill patients compared with those in the control subjects. The changes were present mainly in the patients with sepsis, significant differences between these and the undernourished ones without associated sepsis being observed in glutamine, lysine, tyrosine, valine, leucine, isoleucine, phenylalanine and methionine. The changes were either absent or slight in plasma.
4. The increased concentrations observed in six essential amino acids in the septic patients, but not in those with undernutrition, is consistent with the increased catabolic rate of sepsis.
5. However, the branched-chain amino acids, and lysine, threonine, arginine, and histidine, were present in lower concentrations than might be expected from catabolism, presumably due to utilization. It is suggested therefore that septic patients might benefit from increased proportions of these amino acids in their feeding regimen.
Studies of a Variant Very-Low-Density Lipoprotein with an Acquired Deficiency of Apolipoprotein C-II
Authors: Reckless J. P. D. , Stocks J. , Holdsworth G. , Galton D. J. , Suggett A. J. , Walton K. W. 
Published: August 2015

1. A variant very-low-density lipoprotein was associated with severe hypertriglyceridaemia. Urea—polyacrylamide gel electrophoresis of the tetramethylurea-soluble apolipoproteins of these very-low-density lipoproteins (VLDL) showed that the apolipoprotein C-II content was less than 10% of that in VLDL from hypertriglyceridaemic (3–120 mmol/l) controls.
2. VLDL were incubated with bovine milk lipoprotein lipase (LPL) and a 9,10-3H-labelled triglyceride emulsion. The VLDL deficient in apolipoprotein C-II were a poor activator of LPL, compared with the effect of VLDL with normal content of apolipoprotein C-II obtained from either normal or hypertriglyceridaemic sera.
3. The efficacies of various VLDL as substrates for activated LPL were examined. Apolipoprotein C-II-deficient VLDL were a poor substrate for the activated enzyme compared with normal or hypertriglyceridaemic VLDL, and compared with an artificial triglyceride emulsion.
4. The abnormal VLDL were obtained from a subject with an IgG3 lambda myeloma protein. Intravenous infusion of normal plasma containing apolipoprotein C-II was followed by rapid, complete, but short-lived (5–10 days) clearance of serum triglyceride. The effect was observed on three occasions until treatment of the myeloma was effective.
5. The monoclonal protein behaved as a cryoglobulin, and formed large particle complexes with triglyceride-rich lipoproteins, especially at temperatures below 37°C. The apolipoprotein C-II deficiency, and consequent hypertriglyceridaemia, may be secondary to an autoantibody directed against apolipoprotein C-II. VLDL from relatives with hypertriglyceridaemia, but without myeloma, had normal apolipoprotein content, activated LPL, and were efficient substrates for the enzyme.
Effect of Acute Vasopressin Infusion on Blood Pressure and Plasma Angiotensin II in Normotensive and DOC A—Salt Hypertensive Rats
Authors: Morton J. J. , Del Rio C. Garcia , Hughes Maria J. 
Published: August 2015

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min−1 kg−1 for 1 h into normal, sham-operated and DOCA—salt hypertensive rats. Complete vasopressin/blood pressure dose—response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion.
2. DOCA—salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 ± sd 3.7 fmol/ml) than either the normal (3.9 ± 2.3, P &lt; 0.01) or the sham-operated rats (4.5 ± 2.4, P &lt; 0.01).
3. The DOCA—salt hypertensive rats did not have any detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups.
4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min−1 kg−1, when the plasma concentration was between 30 and 40 fmol/ml.
5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22–23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA—salt hypertensive rats (10.5 ± 2.3, 14.5 ± 4.5 and 8.0 ± 1.6 fmol/ml respectively).
6. These findings suggest that the mechanism of vasopressin involvement in DOCA—salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA—salt hypertension may contribute to the suppression of renin and angiotensin II in this state.
Glutamine Production Rate and its Contribution to Urinary Ammonia in Normal Man
Authors: Golden M. H. N. , Jahoor P. , Jackson A. A. 
Published: August 2015

1. Glutamine [15N]amide was infused at a steady rate of 33.34 μmol/h into seven male adult volunteers who were in the fed state and normal acid-base status.
2. Plasma glutamine amide N enrichment and urinary ammonia N enrichment rose to a constant value within 3 h.
3. The glutamine production rate was 51.8 ± 7.9 mmol/h.
4. The total ammonia excretion rate was 0.87 mmol/h. Of this excreted ammonia 62.6 ± 9% was derived from the amide N atom of glutamine.
5. The excreted glutamine amide N (0.53 mmol/h) was only 1% of the glutamine production. If half the ammonia formed by the kidney is excreted in urine and half liberated into the renal vein in subjects with normal acid-base status [E. E. Owen & R. R. Robinson (1963) Journal of Clinical Investigation, 42, 263–276], then the kidney accounts for only 2% of glutamine disposal.
6. Whole body protein turnover, measured from the urinary [15N]ammonia enrichment, was 30.3 ± 7.7 g of N/day (2.8 g of protein day−1 kg−1).
Baroreceptor Stimulation and Isometric Exercise in Normotensive and Borderline Hypertensive Subjects
Authors: Suarez D. H. , Messerli F. H. , Ventura H. O. , Aristimuno G. , Dreslinski G. R. , Frohlich E. D. 
Published: August 2015

1. The effects of carotid baroreceptor stimulation (neck chamber) on systemic haemodynamics were determined for normotensive and borderline hypertensive subjects during periods of resting and isometric exercise.
2. Both groups reacted to baroreceptor stimulation with a similar decrease in mean arterial pressure and cardiac index at rest and during isometric exercise, but baseline heart rate decreased more in borderline hypertensive patients.
3. Baroreceptor stimulation elicited the same haemodynamic response at rest and during exercise-induced arterial pressure increase. Since the magnitude of arterial pressure had no bearing on the subsequent response, these data suggest resetting of baroreceptors during this short-term blood pressure increase.
Multiple Molecular Forms of Human Heart Cytoplasmic Aspartate Aminotransferase
Authors: Leung F. Y. , Henderson A. R. 
Published: August 2015

1. Cytoplasmic aspartate aminotransferase was isolated and purified from human heart with a final specific activity of 236 units/mg of protein.
2. Three distinct peaks of aspartate aminotransferase activity were detected by isoelectric focusing with isoelectric points of 5.46, 5.60 and 5.71. Two minor subforms were also noted as shoulder patterns with pI 5.2 and 5.8.
3. These electrophoretic characteristics are similar to previous findings of multiple molecular forms detected in human liver and erythrocytes.
Heritability of the Low Density Lipoprotein Receptor Activity of Human Blood Mononuclear Cells: Studies in Normolipidaemic Adult Male Twins
Authors: Weight M. , Cortese C. , Miller U. Sule N. E. , Lewis B. 
Published: August 2015

1. The concordance of low density lipoprotein (LDL) receptor activity of blood mononuclear cells was examined in 26 pairs of monozygotic and 17 pairs of dizygotic normolipidaemic young adult male twins.
2. Receptor activity was quantified as the degradation of 125I-labelled LDL during a 6 h incubation, after derepression of the cells for 72 h in lipoprotein-deficient medium.
3. The total variance of receptor activity was similar in the two groups of twins. In contrast, within-pair variance was five times greater in dizygotic twins than in monozygotic twins (P &lt; 0.001).
4. Estimates of heritability, mostly based on the intra-class correlation coefficients (monozygotic, r = 0.83; dizygotic, r = 0.39), ranged from 0.72 to 1.05.
5. These results suggest that the maximal LDL receptor activity of peripheral cells in normolipidaemic subjects is largely genetically determined.
Urate Does Not Influence the Formation of Calcium Oxalate Crystals in Whole Human Urine at pH 5·3
Authors: Hallson P. C. , Rose G. A. , Sulaiman S. 
Published: August 2015

1. Samples of fresh human urine were treated with immobilized uricase to lower urate concentration. Urate was added to yield low, normal and high urate samples.
2. Each sample was rapidly evaporated at pH 5.3 to standard osmolality and the yield of calcium oxalate crystals measured either by semi-quantitative microscopy or fully quantitative radioisotope techniques.
3. Increase of urinary urate did not increase the calcium oxalate crystals formed and may even have had an opposite effect.
4. Allantoin was without significant effect upon calcium oxalate crystal formation.
5. These data provide no support for the suggestion that reducing urate concentrations in the urine may be of value in treatment of patients with calcium oxalate stones.
Absence of Activation in Vitro of Renin in Rat Plasma
Authors: De Keijzer M. H. , Provoost A. P. , Derkx F. H. M. 
Published: August 2015

1. Rat plasma was subjected at 4°C to various treatments known to convert inactive renin into its active form in human plasma.
2. No statistical differences in plasma renin concentration were found when the levels after the various treatments were compared with that of untreated rat plasma.
3. It is concluded that, in contrast to human plasma, no inactive form of renin is present in rat plasma.
The Renin-Angiotensin-Aldosterone System, Antidiuretic Hormone and Sympathetic Nerve Activity in an Experimental Model of Congestive Heart Failure in the Dog
Authors: Riegger A. J. G. , Liebau G. 
Published: August 2015

1. Congestive heart failure was induced in dogs by rapid pacemaker stimulation of the heart (240–280/min) for 14 days. This represents a model of low output heart failure which permits the study of the development and reversal of congestive heart failure in an anatomically intact circulation in the unanaesthetized animal.
2. Cardiac output was reduced by 54%. Pulmonary artery pressure gradually increased by a facter of 2.4 and pulmonary capillary pressure rose to 4.6 times basal values. The animals retained a mean of 1.1 litres of fluid.
3. At the same time there was a gradual increase of plasma levels of renin, angiotension II, aldosterone, noradrenaline and adrenaline. After the pacemaker stimulation was discontinued all hormone levels returned to normal, the retained fluid was excreted, and intracardiac pressures and cardiac output returned to baseline values.
4. When heart failure was established at the end of the pacemaker stimulation period an inappropriately high secretion of antidiuretic hormone in relation to plasma osmolality was observed in five of six dogs.
5. It is concluded that beside the well-known non-hormonal renal factors, these hormone systems-5-be involved in the formation of oedema in congestive heart failure. The inappropriately high levels of antidiuretic hormone-5-cause hyponatraemia by water retention, representing a state of ‘dilutional hypo-osmolality’.