bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Prostaglandin E2 and Prostaglandin F2α Upon Urinary Kallikrein Excretion in Rats
Authors: Croxatto H. R. , Arriagada R. , Rojas M. , Roblero J. , Rosas R. 
Published: August 2015

1. In normally hydrated rats prostaglandin F2α (PGF2α) in doses of 5 μg/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2·5% of body wt. with 0·5% NaCl solution, PGF2α produced similar changes in kallikrein activity and electrolyte excretion.
2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion.
3. PGE2 in doses of 5, 12·5 and 25 μg/100 g body wt. in overhydrated rats given 2·5% and 0·5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose.
4. PGF2α, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose.
5. The different actions of PGE2 and PGF2α may be part of a regulatory mechanism associated with the kallikrein—kinin system which contributes maintainance of extracellular fluid homeostasis.
Evidence for an Unidentified, Adrenocorticotrophic Hormone-Dependent Mineralocorticoid Maintaining Hypertension in Young Women with Hypoaldosteronism
Authors: Hoefnagels W. H. L. , Drayer J. I. M. , Hofman J. A. , Smals A. G. H. , Benraad TH. J. , Kloppenborg P. W. C. 
Published: August 2015

1. Pronounced hypoaldosteronism was found in five young women with low-renin hypertension and characteristic features of the mineralocorticoid hypertensive syndrome.
2. There was no overproduction of the mineralocorticoids 11-deoxycorticosterone and 18-OH-11-deoxycorticosterone.
3. Dexamethasone restored blood pressure to normal, decreased body weight, increased plasma potassium, and increased plasma renin activity and aldosterone excretion in all patients.
4. The data suggest overproduction of an unknown adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in these patients.
Long-Term Treatment of Hypertension in Man by an Orally Active Angiotensin-Converting Enzyme Inhibitor
Authors: Brunner H. R. , Gavras H. , Turini G. A. , Waeber B. , Chappuis P. , McKinstry D. N. 
Published: August 2015

1. Captopril or SQ 14 225, administered orally twice a day, reduced the blood pressure of hypertensive patients whatever their clinical diagnosis and even when their plasma renin activity was ‘normal’ or low.
2. Long-term administration of captopril, either alone or together with diuretics, provides a powerful new tool with which to treat ambulatory hypertensive patients.
3. The renin system may play an important role in maintaining blood pressure in a majority of hypertensive patients.
β-Adrenoreceptor-Blocking Agents and Lipid Metabolism
Authors: England J. D. F. , Hua A. S. P. , Shaw J. 
Published: August 2015

1. Chlorothiazide twice a day plus atenolol, metoprolol, pindolol and propranolol in single daily doses administered to patients with essential hypertension achieved effective control of blood pressure.
2. Each β-adrenoreceptor-blocking drug was associated with small, but significant, increases in plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.
Low-density Lipoprotein Turnover Studies in Man. Evaluation of the Integrated Rate Equations Method, Use of a Whole-body Radioactivity Counter, and the Problem of Partial Denaturation
Authors: Calvert G. D. , James H. M. 
Published: August 2015

1. We studied the turnover of low-density lipoprotein, density 1·031–1·056 kg/l, in five normal subjects and in four subjects with hyperlipoproteinaemia, using as tracer low-density lipoprotein labelled in the protein moiety with 131I. We analysed data derived with and without a whole-body radioactivity counter. Four models were used, including the integrated rate equations of Nosslin.
2. In most patients all methods gave similar results for the fractional catabolic rate. Use of the integrated rate equations allowed us to calculate the fractional catabolic rate in 3–5 days compared with 12 days for a multicompartmental method using plasma activity alone. The integrated rate equations method was valid only in a steady metabolic state, and could apparently be used when there was minor tracer denaturation. It was probably invalid when there was major partial tracer denaturation. The degree of partial denaturation could be estimated from the whole-body radioactivity graph. The whole-body counter was quick to use, required low levels of radioactivity and avoided error-prone urine collection.
3. Estimates of the relative size of the intravascular and extravascular compartments derived by five different methods were similar in studies in which there was insignificant denaturation of tracer.
Presence of Apolipoprotein-CII in Commercially available Albumin Fractions
Authors: Östlund-Lindqvist Ann-Margret , Boberg J. 
Published: August 2015

1. Commercially available bovine serum albumin as Cohn fraction V was demonstrated to contain small amounts of apolipoprotein-CII.
2. This apolipoprotein activated lipoprotein lipase in the same way as apolipoprotein-CII purified from human very-low-density lipoproteins.
Loss of Metacarpal and Iliac Bone in Chronic Renal Failure: Influence of Haemodialysis, Parathyroid Activity, Type of Renal Disease, Physical Activity and Heparin Consumption
Authors: Henderson R. G. , Russell R. G. G. , Earnshaw M. J. , Ledingham J. G. G. , Oliver D. O. , Woods C. G. 
Published: August 2015

1. Bone loss was assessed by measurement of cortical thickness of metacarpal bone by X-ray and of trabecular bone area in serial bone biopsies in 49 patients with chronic renal failure, six before and 45 during maintenance haemodialysis treatment.
2. Metacarpal cortical measurements (MCM) were very reproducible (coefficient of variation 1·95%), whereas bone area measurements by histology showed great variability. There was no correlation between rates of change of MCM and bone area over the same period, although both tended to fall with time.
3. The mean annual rate of bone loss measured by MCM for patients on dialysis was 2·08 ± 0·32 mm/year (mean ±1 sem) and this rate was not significantly different from the mean rate of loss of 2·49 ± 0·78 mm/year for the six patients who were not on maintenance haemodialysis. 61% of all patients showed a significant decrease during the period of study (1–6 years), but none had symptoms attributable to bone loss.
4. The loss tended to be greatest in women over the age of 40 years. The initial amount of bone and the rate of loss measured by MCM or bone histology were not influenced significantly by the presence or absence of histological or radiological evidence of parathyroid overactivity or of osteomalacia, nor by differences in the causes of renal disease.
5. Loss of metacarpal cortical bone correlated with heparin consumption during haemodialysis in men but not in women. The amount of bone and its rate of loss was not influenced by the presence of an arteriovenous shunt in one arm compared with the other. In neither sex did bone loss correlate with physical activity.
6. A relative deficiency of calcium due to a low dietary calcium intake and intestinal malabsorption of calcium, together with a dialysate calcium of only 1·5 mmol/l, may be more important causes of bone loss in patients in this study.
Sequential Enzyme and Subcellular Fractionation Studies on Jejunal Biopsy Specimens from Patients with Post-Infective Tropical Malabsorption
Authors: Peters T. J. , Jones P. E. , Wells G. , Cook G. G. 
Published: August 2015

1. Jejunal biopsy specimens were obtained from seven patients with post-infective tropical malabsorption, four of whom were infected with Giardia lamblia.
2. Enzymic analysis of the biopsy homogenates revealed a selective reduction of certain enzymes (alkaline phosphatase, γ-glutamyl transferase) localized at least in part to the brush border. Other enzymes (leucyl-2-naphthylamidase, α-glucosidase) were unaffected.
3. Density gradient centrifugation confirmed the selective decrease in the brush-border activity but the equilibrium density of the organelle was normal. Homogenization studies revealed that the brush border was unusually fragile.
4. Apart from reduced activities of the basal—lateral marker enzyme 5′-nucleotidase and enhanced lysosomal fragility, other organelles showed normal properties. There were no significant differences in any of these parameters in the patients with or without giardiasis.
5. The patients were restudied after their jejunal morphology and clinical features had returned to normal. All these parameters, apart from a persistently reduced activity of 5′-nucleotidase, returned to normal.
6. It is suggested that the principal lesion in patients with post-infective tropical malabsorption affects the cell membrane, specifically affecting the absorptive—digestive capacity of the enterocyte. These findings suggest that there is direct brush-border damage rather than mucosal invasion by bacteria, viruses or Giardia lamblia.
l-Asparaginyl-Trna Synthetase and l-Asparagine Synthetase Activities of l-Asparaginase-Sensitive and -Resistant Forms of the Mouse Gardner Lymphoma 6C3HED
Authors: Davies M. R. , Lambert Lucy P. , Marshall R. D. 
Published: August 2015

1. The mouse Gardner lymphoma 6C3HED was grown in ascites fluid in a form sensitive to the action of l-asparaginase (line 1), in another form which was resistant to l-asparaginase (line 2) and in a third form with partial sensitivity to l-asparaginase (line 3).
2. The l-asparaginyl-tRNA synthetase activities of extracts of the tumour cells, cultured both in the mouse and in vitro, were determined. Two of the lines, 1 and 3, in early passage numbers, showed a derepression mechanism involving l-asparagine. Mutation occurred with these lines resulting in the l-asparaginyl-tRNA synthetase activity of all the tumour cell lines being the same.
3. Cells of line 1 had low l-asparagine synthetase activity, which was unchanged by altering the supply of l-asparagine in vitro. Cells of lines 2 and 3 exhibited l-asparagine synthetase activities, which changed with the supply of l-asparagine.
4. It is not certain that l-asparagine synthetase activity of l-asparaginase-sensitive cells is controlled by l-asparaginyl-tRNA acting as a corepressor.
Effect of Intravenous Sodium Lactate on Renal Tubular Reabsorption of Phosphate in Man
Authors: Walton R. J. 
Published: August 2015

1. The effects of sodium dl-lactate and sodium chloride (2·5 mg/kg as 865 mmol/l solutions given by intravenous infusion over 20 min) on the renal tubular reabsorption of phosphate have been compared in five normal adults.
2. Sodium lactate produced a marked but transient increase in urinary phosphate excretion due to a reduction in net renal tubular reabsorption of phosphate; the mean value of the maximum rate of renal tubular reabsorption of phosphate/unit of glomerular filtration rate (TmP/GFR) decreased from 1·14 to 0·82 mmol/l.
3. This effect was not due simply to expansion of the volume of the extracellular fluid, since the reduction in TmP/GFR after sodium chloride infusion was less marked, nor did it seem to be due entirely to alkalinization of the urine since the maximum increase in urinary pH occurred 20–40 min after the maximum decrease in TmP/GFR.
Effect of Indomethacin on Blood Pressure in the Normotensive Unanaesthetized Rabbit: Possible Relation to Prostaglandin Synthesis Inhibition
Authors: Colina-Chourio J. , McGiff J. C. , Nasjletti A. 
Published: August 2015

1. To test the hypothesis that endogenous prostaglandins contribute to the regulation of blood pressure, we studied the effect of an inhibitor of prostaglandin synthesis, indomethacin, on mean aortic blood pressure in the normotensive, unanaesthetized rabbit.
2. Daily administration of indomethacin at 42 μmol/kg subcutaneously, but not of vehicle only, for 14 consecutive days, elevated the average mean arterial pressure in seven rabbits from 88 ± 3 mmHg on the last day of the control period to 105 + 3 mmHg (P &lt; 0·01) and 107 ± 2 mmHg (P &lt; 0·01) on days 6 and 14 of indomethacin treatment respectively, and reduced the urinary excretion of prostaglandin-like substance from 1·06 ± 0·26 to 0·17 ± 0·05 nmol of prostaglandin E2 equivalents/ day (P &lt; 0·05; n = 5). Neither indomethacin nor the vehicle affected the intake of water, the 24 h urine volume, the cumulative difference between sodium intake and urinary sodium excretion, or the plasma volume.
3. The results of the study are compatible with the hypothesis that one or more prostaglandins contribute to maintain normotension in the rabbit and that reduction in prostaglandin biosynthesis may cause blood pressure to rise.
Carbon Dioxide Equilibration in Canine Lungs during Rebreathing and Acute Alkalosis
Authors: Latimer R. D. , Laszlo G. 
Published: August 2015

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe.
2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe.
3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood.
4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts.
5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.
Gilbert's Syndrome: Analytical Subcellular Fractionation of Liver Biopsy Specimens. Enzyme Activities, Organelle Pathology and Evidence for Subpopulations of the Syndrome
Authors: Dawson J. , Seymour C. A. , Peters T. J. 
Published: August 2015

1. The hepatic organelle pathology of 12 patients with Gilbert's syndrome was studied by analytical subcellular fractionation in combination with enzymic microanalysis of liver biopsy material.
2. All patients showed increased activities of the endoplasmic reticulum marker enzyme, neutral α-glucosidase. Seven patients showed a decrease in the modal density of the endoplasmic reticulum, from 1·20 to 1·15 g/ml. These patients also showed striking hypertrophy of the hepatocyte smooth endoplasmic reticulum on electron microscopy. The remaining five patients showed normal endoplasmic reticulum density distribution with a peak at 1·20 g/ml, and had normal appearance of the endoplasmic reticulum on electron microscopy.
3. All patients showed increased activity of three lysosomal marker enzymes: N-acetyl-β-glucosaminidase, acid phosphatase and β-glucuronidase. The distribution of these enzymes in the sucrose gradients showed less enzyme in the high-density region of the gradients, indicating a reduced equilibrium density of the lysosomes. Assays of latent and sedimentable N-acetyl-β-glucosaminidase, a measure of lysosomal integrity, were normal.
4. Marker enzyme activities and density gradient distribution of other organelles, including plasma membrane (5′-nucleotidase), mitochondria (malate dehydrogenase), biliary canaliculi (γ-glutamyl transferase) and cytosol (lactate dehydrogenase) were normal. Increased catalase activities were noted.
Release of Dipeptide Hydrolase Activities from Rat Small Intestine Perfused in Vitro and in Vivo
Authors: Gardner M. L. G. , Plumb Jane A. 
Published: August 2015

1. Hydrolase activities against three dipeptides were measured in mucosal cytoplasm in unperfused intestines and in mucosal cytoplasm, luminal effluents and serosal secretions after perfusion in vitro and in vivo for 1 h. Intestines in vitro were prepared both from anaesthetized rats and from freshly killed rats.
2. Only 0·6–1·9% of the initial cytoplasmic activity was recovered in the luminal effluent when intestines in vitro were prepared from anaesthetized rats. Recoveries in luminal effluents were similar (1·3–3·3%) during perfusion in vivo.
3. Losses of dipeptidases into the luminal effluent were four to eight times greater when intestines in vitro were prepared from freshly killed animals.
4. Similar losses of dipeptidases into the secretion on to the serosal surface were observed; they too were much greater when intestines were prepared from freshly killed animals.
5. Small losses of mucosal DNA during perfusion were also observed; however, losses of cytoplasmic peptidases were consistently slightly greater.
6. Enzyme loss therefore probably occurs both by sloughing of whole cells and by a more specific process which is greatly influenced by experimental procedure. Caution is necessary in the interpretation of peptide transport experiments in vitro, although the possibility that intraluminal hydrolysis is of physiological significance must not be excluded.
Muscle Protein Degradation in Premature Human Infants
Authors: Ballard F. J. , Tomas F. M. , Pope L. M. , Hendry P. G. , James B. E. , MacMahon R. A. 
Published: August 2015

1. Myofibrillar protein degradation has been measured by the rate of 3-methylhistidine excretion in premature infants weighing between 635 g and 1295 g. Analyses were made in conjunction with 1–3 day nitrogen balance studies.
2. In 56 balance studies in 36 infants, total muscle protein breakdown varied between 0·70 and 2·58 (mean 1·05) g day−1 kg−1 body weight while the percentage of total muscle protein degraded each day was between 3·3 and 8·3 (mean 4·8).
3. Both total and fractional rates of protein breakdown showed highly significant negative correlations with nitrogen retention but no relationship to total energy input.
4. Protein degradation was higher than average in infants who were losing weight at the time of the balance study, lower in infants who were gaining weight and higher in those who died within 2 weeks of the analysis.
5. Myofibrillar protein breakdown was not different between infants fed orally and those receiving total parenteral nutrition.
6. Generally the effects of nitrogen and energy status on muscle protein degradation in the premature infants are different from changes reported in adult human beings or adult rats. We suggest that this difference may be a consequence of the very limited energy reserves of the premature infant.
Haemodynamic Profile of Angiotensin II Antagonism in Essential Hypertensive Patients
Authors: Hunyor S. N. , Larkin H. , Rowe Janet 
Published: August 2015

1. The haemodynamic response to antagonistic (10 μg min−1 kg−1) and agonistic (40 μg min−1 kg−1) doses of saralasin was studied in young essential hypertensive patients. Blood pressure behaviour alone was thought to be inadequate to describe the response pattern.
2. Pre-saralasin setting of the renin-angiotensin axis was varied with salt intake (15 and 290 mmol of Na+/day) each for 10 days. This failed to influence blood pressure or plasma volume.
3. Antagonist blockade after low salt lowered blood pressure in three patients with the highest plasma renin values. Cardiac output rose in two of these, but it dropped in all others.
4. Decreases in cardiac output occurred with both doses of saralasin and even with suppression of the renin-angiotensin axis. This response is therefore unlikely to be due to removal of myocardial or venous angiotensin effects.
5. The renin-angiotensin system played a part in maintenance of blood pressure only with severe salt restriction and in a small proportion of cases.
6. No heart rate effect was seen with saralasin.
7. Blood pressure and total peripheral resistance responses were dependent on pre-(antagonist/ agonist) setting, but heart rate and cardiac output were not influenced by this factor.
Recordings of Renal and Splanchnic Sympathetic Nervous Activity in Normotensive and Spontaneously Hypertensive Rats
Authors: Thorén P. , Ricksten S.-E. 
Published: August 2015

1. Recordings have been obtained from single sympathetic fibres to the left kidney in anaesthetized adult spontaneously hypertensive (SH) rats and Wistar—Kyoto normotensive (WK) rats.
2. Under control conditions SH rats had a mean sympathetic activity of 3·3 ± se 0·45 Hz and WK rats 1·6 ± 0·23 Hz. During noradrenaline infusion single fibre discharge decreased graudally to low levels in both SH and WK rats. The absolute decrease in fibre activity/mmHg rise of arterial pressure was greater in SH rats than in WK rats, but the reverse was true when the discharge reduction was expressed as a percentage change.
3. Recordings have also been obtained from the left splanchnic nerve in awake SH and WK rats. Upon volume load with blood, in SH rats the sympathetic activity decreased significantly more than in WK rats.
4. Thus the sympathetic discharge to the kidneys is higher in SH rats than in WK rats. Upon volume load SH rats show an exaggerated reflex response, probably due to an augmented volume-receptor response.
Absence of Sympathetic Cholinergic Vasodilatation in Cats during Early Stages of Affective Behaviour Elicited by Stimulation of Central Amygdala, Postero—Lateral Hypothalamus and Locus Coeruleus
Authors: Stock G. , Stumpf H. , Schlör K. H. 
Published: August 2015

1. Stimulation of the central amygdala, posterolateral hypothalamus and locus coeruleus in cats resulted in a sustained increase in arterial pressure, an increase in heart rate, with a poststimulation bradycardia and an increase in peripheral resistance (vasoconstriction in the vessels of the hindlimbs). The behavioural pattern was characterized by an alerting reaction. Increased stimulus intensities resulted in rage reactions if the amygdala or the hypothalamus were stimulated.
2. Stimulation of the basal amygdala resulted in a cardiovascular pattern characterized by a sympathetic cholinergic vasodilatation. The concomitantly observed behaviour was characterized by alerting, anxious behaviour, eventually resulting in defence.
3. Alerting was not necessarily linked to sympathetic cholinergic vasodilatation.
4. The cardiovascular pattern including sustained vasoconstriction of the vessels of the hindlimbs was supposed to be of greater importance for the induction of hypertension than the cardiovascular pattern, including sympathetic cholinergic vasodilatation.
Low Urinary Kallikrein Excretion and Elevated Blood Pressure Normalized by Orally Applied Kallikrein in Essential Hypertension
Authors: Overlack A. , Stumpe K. O. , Ressel C. , Krück F. 
Published: August 2015

1. Urinary kallikrein was measured in 67 patients with essential hypertension and 25 normotensive subjects variously on unrestricted and low sodium diet. Also, the effect of orally applied hog pancreatic kallikrein on elevated blood pressure and kallikrein excretion was evaluated.
2. Urinary kallikrein was reduced in a large subgroup of patients with sustained essential hypertension.
3. With salt restriction, urinary kallikrein rose markedly in normotensive subjects and patients with borderline hypertension but not in those with sustained hypertension.
4. Oral kallikrein normalized reduced kallikrein excretion and lowered elevated blood pressure.
5. The rise in urinary kallikrein with oral kallikrein was due to an increased formation of endogenous enzyme.
6. A defective kallikrein—kinin system may be involved in both the low urinary kallikrein excretion and the hypertension.