bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sodium Excretion and Blood Pressure in Essential Hypertensive Patients during the Early Phase of Hospital Admission
Authors: De Leeuw P. W. , Wester A. , Van Soest G. A. W. , Vaarties-Steeman J. E. M. , Birkenhäger W. H. 
Published: August 2015

1. In 91 essential hypertensive patients cumulative sodium balance was studied during the first week after they were taken into hospital. Sodium intake was fixed at 55 mmol/day.
2. After the first week, when sodium equilibrium was achieved, haemodynamic and endocrinological studies were carried out (cardiac output, renal plasma flow, plasma volume, measurements of plasma concentrations of total and active renin, aldosterone and noradrenaline).
3. On the basis of cumulative sodium balance a discrimination could be made between three groups. Group I (23 patients) accumulated sodium (52 mmol) before attaining equilibrium; group II (35 patients) were in balance from the beginning; group III (33 patients) exhibited a negative balance and lost on the average 125 mmol before equilibrium was attained.
4. On admission blood pressure and other characteristics were similar in the three groups. The decrease in blood pressure over the first 24 h period was equal. After that, the group characterized by a negative cumulative sodium balance (III) continued to exhibit a fall in blood pressure whereas groups I and II did not.
5. After sodium equilibrium had been attained, the haemodynamic profiles were somewhat different between groups. Group I (with a positive balance) showed greater systemic and renal vascular resistances than the other groups.
6. It is concluded that sodium loss contributes to the decrease in blood pressure on the second day of hospital admission and after. The blood pressure reduction during the first day is due to an independent mechanism, e.g. a decrease in sympathetic nervous tone.
7. It is also apparent that the attainment of sodium equilibrium during clinical investigations constitutes no guarantee that subjects are physiologically comparable; the preceding sodium balance has to be taken into account.
Antihypertensive Effects of Clonidine in Tetraplegic Subjects Devoid of Central Sympathetic Control
Authors: Mathias C. J. , Reid J. L. , Wing L. M. H. , Frankel H. L. , Christensen N. J. 
Published: August 2015

1. The effects of 300 μg of oral clonidine on blood pressure, heart rate, plasma noradrenaline and adrenaline concentrations were studied in seven tetraplegic subjects with physiologically complete cervical spinal cord transections.
2. Clonidine did not significantly change resting blood pressure during the 8 h of the study. Resting heart rate fell. Resting plasma noradrenaline and adrenaline concentrations, when measured 2 h after clonidine, were not significantly lower.
3. Urinary bladder stimulation resulted in a marked rise in blood pressure accompanied by an elevation in plasma noradrenaline but not adrenaline. The hypertensive response to bladder stimulation was substantially reduced by clonidine, the maximum suppression occurring 2–4 h after administration of the drug. The plasma noradrenaline response to bladder stimulation, when measured 2 h after clonidine, was significantly lower than the response before clonidine. In two tetraplegic subjects with indwelling catheters the rise in intravesical pressure caused by bladder stimulation was unchanged by clonidine.
4. The pressor response to intravenous noradrenaline in two tetraplegic subjects and to intravenous phenylephrine in a further two tetraplegic subjects was unchanged by clonidine.
5. Clonidine may have additional antihypertensive effects which occur independently of actions in the brain. These effects may be exerted by an action either on sympathetic neurones in the spinal cord or on presynaptic α-adrenoreceptors in the periphery.
The Evidence that Salt is an Important Aetiological Agent, If Not the Cause, of Hypertension
Authors: Morgan T. , Myers J. , Carney S. 
Published: August 2015

1. Salt intake and the incidence of hypertension correlate between populations.
2. Salt intake within a population may correlate with the incidence of hypertension.
3. Disorders that lead to retention of salt cause hypertension.
4. Modest salt restriction reduces blood pressure in many patients.
5. Reducing salt balance and preventing the compensatory rise in angiotensin II controls blood pressure in most patients.
6. Salt is the probable cause of the epidemic of hypertension in the Western world; this could be prevented by salt restriction.
Baroreflex Sensitivity in Renal Failure
Authors: Tomiyama Osamu , Shiigai Tatsuo , Ideura Terukuni , Tomita Kimio , Mito Yasuyoshi , Shinohara Shinsuke , Takeuchi Jugoro 
Published: August 2015

1. Baroreflex sensitivity was evaluated in 22 non-dialysed patients with chronic renal failure secondary to chronic glomerulonephritis. Baroreflex sensitivity was judged by the slope of the linear regression of the pulse interval on the rise in systolic blood pressure with injection of phenylephrine or reduction by amyl nitrite inhalation.
2. Baroreflex sensitivity was reduced in these patients as compared with normal controls. Reduction of baroreflex sensitivity was significantly greater in nine hypertensive than 13 normotensive patients with chronic renal failure.
3. A significant positive correlation was found between baroreflex sensitivity and motor nerve conduction velocity measured on ulnar nerve in 13 patients examined.
4. Saline was given with high dietary salt intake to seven normotensive patients with chronic renal failure for 2 or 5 days in order to determine whether the severe depression of baroreflex sensitivity can be an initiating factor for hypertension. Blood pressure was raised to hypertensive levels within 5 days in two patients in whom baroreflex sensitivity was nearly as low as that of hypertensive patients, but not in five cases whose baroreflex sensitivity was normal or only mildly depressed. Plasma volume increased to the same degree in both groups. Baroreflex sensitivity did not change in the former two cases despite blood pressure elevation.
5. It is concluded that reduced baroreflex sensitivity in chronic renal failure correlated with the presence of hypertension, as well as uraemic neuropathy, and may be one of the pathogenetic mechanisms of hypertension in end-stage chronic glomerulonephritis.
Sieving Studies in ‘Urea-Induced Nephropathy’ in the Dog
Authors: Vanrenterghem Y. , Vanholder R. , Lammens-Verslijpe M. , Lambert P. P. 
Published: August 2015

1. The intrarenal infusion of concentrated urea after clamping of the renal artery produced immediate proteinuria in the dog. The predominant lesion on ultramicroscopy was destruction of the epithelial layer. Colloidal iron staining showed decreased fixed anionic charges in the capillary wall.
2. Sieving studies with neutral macromolecules such as 125I-labelled polyvinylpyrrolidone and [3H]-dextran or an electronegatively charged polymer, [3H]dextran sulphate, showed a moderate increase in permeability to the neutral tracers and a much more severe alteration of the electrostatic barrier to the anionic polymer. The fractional clearance of dextran sulphate molecules increased to a greater extent than clearance of neutral dextrans of comparable size.
3. The shape of the curve relating the fractional clearance of dextran sulphate to molecular size is also modified in the contralateral kidney. This may be due to elevated plasma angiotensin II concentrations.
The Relationship between Plasma Biotin Concentration and Circulating Leucocyte β-Methylcrotonyl-CoA Carboxylase and Propionyl-CoA Carboxylase
Authors: Bartlett K. , Horsburgh T. , Gompertz D. 
Published: August 2015

1. A newly developed biotin assay was used to monitor plasma and urinary biotin concentration after the oral administration of biotin.
2. In two normal subjects, leucocyte propionyl-CoA carboxylase and β-methylcrotonyl-CoA carboxylase were markedly stimulated after the administration of biotin.
An Association between Plasma Progesterone and Erythrocyte Carbonic Anhydrase I Concentration in Women
Authors: Paciorek J. , Spencer N. 
Published: August 2015

1. Erythrocyte carbonic anhydrase I was measured by immunoelectrophoresis in blood samples taken at intervals during the menstrual cycle of 26 normal women. Plasma progesterone concentrations were also measured in 18 of these subjects. In every case, the erythrocyte carbonic anhydrase I concentration reached a maximum at that point in the cycle when there was maximum secretion of progesterone. Statistical analysis indicated that the observed changes in erythrocyte carbonic anhydrase I concentration are highly significant and that erythrocyte carbonic anhydrase I and plasma progesterone concentrations are significantly correlated.
2. In three pregnant subjects the erythrocyte carbonic anhydrase I concentration showed a steady increase up to term.
3. Women taking progestogens in contraceptive pills, in doses of 1 mg/day or greater, had significantly higher concentrations of erythrocyte carbonic anhydrase I compared with females receiving no medication.
4. These observations strongly suggest that there may be a causal connection between plasma progesterone concentration and erythrocyte carbonic anhydrase I concentration in women.
Influx of Glycylsarcosine and l-Lysyl-l-Lysine into Hamster Jejunum in Vitro
Authors: Taylor E. , Burston D. , Matthews D. M. 
Published: August 2015

1. This paper reports an investigation of whether the dipeptides glycylsarcosine and l-lysyl-l-lysine share a single mediated transport mechanism into hamster jejunum, or whether one of these peptides is taken up in part by a mediated mechanism unavailable to the other. The investigation, using rings of everted jejunum in vitro, was carried out at pH 5 in order to reduce brush border and/or intramedium hydrolysis of lysyl-lysine.
2. The kinetics of uptake of each peptide was studied over a wide range of concentrations. Estimates of the simple diffusion component in uptake of each peptide were made by the method of self-inhibition of transport as previously described. After correction for simple diffusion, uptake of each peptide conformed to Michaelis-Menten kinetics, and values for Kt and Vmax. were obtained.
3. It was found that each peptide was capable, at infinitely high concentration, of complete inhibition of mediated uptake of the other. The inhibitory effect was competitive. We concluded that glycylsarcosine and lysyl-lysine were taken up by a common mediated mechanism (or possibly mechanisms), neither peptide being taken up by a mediated mechanism unavailable to the other.
4. A previous paper showed that l-glutamyl-l-glutamic acid and glycylsarcosine were taken up by a common mediated mechanism, and this paper shows that l-lysyl-l-lysine and glycylsarcosine are taken up by a common mediated mechanism. It is therefore postulated that the neutral dipeptide glycylsarcosine, the acidic dipeptide glutamyl-glutamic acid and the basic dipeptide lysyl-lysine all share a common mediated mechanism for uptake. This suggests that peptide uptake differs from amino acid uptake in that it is indifferent to the net charge on the amino acid side chain(s).
Estimation of Cardiac Output from the Rate of Change of Alveolar Carbon Dioxide Pressure during Rebreathing
Authors: Winsborough Mary , Miller J. N. , Burgess D. W. , Laszlo G. 
Published: August 2015

1. A new CO2-rebreathing method for estimating cardiac output is described, and compared with a method employing N2O performed at the same time.
2. The subject inhales from a reservoir of 30% O2 in N2 and rebreathes into and out of an empty bag for 10s.
3. Oxygenated mixed venous Pco2 is then determined by rebreathing 7–15% CO2 in O2, the mixture being selected to obtain a plateau of CO2 concentration.
4. Pco2 rises exponentially towards the plateau value during the rebreathing of 30% O2. Cardiac output is calculated from the rate of change of the alveolar—mixed venous Pco2 difference by a differential version of the Fick equation employing published CO2 dissociation curves for whole blood in vitro.
5. The slope of the regression of cardiac output on V̇o2 is similar to that obtained in other studies employing direct Fick measurements. The slope is some 15% greater than obtained with N2O but the difference is significant only when Oz consumption is greater than 2 litres/min.
6. The CO2 dissociation slope of blood does not differ during pulmonary gas exchange in vivo from that determined at equilibrium in vitro.
7. The volume of pulmonary blood available for CO2 exchange may rise to about 1 litre in heavy exercise, with a transit time of 1–2 s in the lungs.
8. The method can be employed for estimating pulmonary blood flow during physiological studies in subjects with normal lungs.
The Role of Prostaglandins in Glucagon-Induced Natriuresis
Authors: Kirschenbaum M. A. , Zawada E. T. 
Published: August 2015

1. Three groups of anaesthetized dogs were studied to determine the role of renal prostaglandins in glucagon-induced natriuresis.
2. Urine flow, sodium and prostaglandin E excretion rates increased significantly in the experimental kidney with glucagon infusion (0.20 μg/min) into the renal artery. These changes were completely reversed after the administration of either of two inhibitors of prostaglandin synthesis.
3. Infusion of glucagon (0.20 μg/min) after the administration of either of the prostaglandin synthetase inhibitors failed to increase either urine flow rate or sodium excretion above control values and failed to elevate urine prostaglandin E excretion rates.
4. Infusion of glucagon (0.75–1.25 μg/min) resulted in significant elevations in urine flow rate, glomerular filtration rate, renal plasma flow, urine sodium and prostaglandin E excretion rates.
5. The data presented indicate that the diuresis and natriuresis seen with the infusion of glucagon (0.20 μg/min) are accompanied by an increase in urine prostaglandin E excretion and are reversed by the administration of inhibitors of prostaglandin synthesis, suggesting that the increased urine flow and sodium excretion rates are dependent on prostaglandin-mediated mechanisms. The administration of glucagon in higher doses appears to be associated with alterations in electrolyte excretion and glomerular filtration rate, which presumably is related to factors other than prostaglandin synthesis and release.
Insulin-Induced Renin Release: Blockade by Indomethacin in the Rat
Authors: Campbell W. B. , Zimmer Judith A. 
Published: August 2015

1. Since prostaglandins appear to mediate adrenergically stimulated renin release, the effect of indomethacin was examined on insulin-induced renin and catecholamine release in conscious rats. Insulin (10 units/kg subcutaneously) increased plasma renin activity from 2.8 ± 0.5 to 9.0 ± 1.1 pmol h−1 ml−1 (P&lt;0.001) while also increasing plasma adrenaline, noradrenaline and the urinary excretion of prostaglandin E2 and F2α. Plasma potassium and glucose were reduced by 16 and 54%respectively.
2. Indomethacin (14 μmol/kg subcutaneously) reduced the urinary excretion of prostaglandin E2 and F2α by 67 and 54%respectively, without altering the other parameters.
3. Indomethacin inhibited insulin-induced renin release by 67%(P&lt;0.01) and blocked the insulin-induced increases in urinary postaglandin E2 and F2α. The insulin-induced changes in plasma catecholamines, potassium and glucose were unaltered by indomethacin.
4. These findings suggest that renal prostaglandins mediate this form of adrenergically stimulated renin release by acting at a site distal to the β-adrenoreceptor.
Identification of Two Types of Porphyria Cutanea Tarda by Measurement of Erythrocyte Uroporphyrinogen Decarboxylase
Authors: Elder G. H. , Sheppard Diane M. , De Salamanca R. E. , Olmos A. 
Published: August 2015

1. Erythrocyte uroporphyrinogen decarboxylase activity has been measured in 27 patients with porphyria cutanea tarda, of whom 11 had a family history of overt porphyria cutanea tarda.
2. Eight patients from six families had erythrocyte uroporphyrinogen decarboxylase activities that were decreased to about half of control values. This decrease was shown by family studies to be inherited as an autosomal dominant characteristic. Two of these patients had no family history of overt porphyria cutanea tarda.
3. Nineteen patients had uroporphyrinogen decarboxylase activities close to or within the range found in 18 control subjects. Of these, five patients had a family history of porphyria cutanea tarda.
4. Inheritance of an autosomal dominant gene which decreases uroporphyrinogen decarboxylase activity in erythrocytes and liver is an uncommon cause of porphyria cutanea tarda and may not explain all cases of familial porphyria cutanea tarda. The hepatic enzyme defect in the common type of porphyria cutanea tarda, in which erythrocyte uroporphyrinogen decarboxylase activity is normal, may be caused either by inheritance of a gene whose effect is restricted to the liver or by chemicals that selectively inhibit the hepatic enzyme.
Metabolic Effects of the Use of Protein-Sparing Infusions in Postoperative Patients
Authors: Foster K. J. , Alberti K. G. M. M. , Binder C. , Hinks Leslie , Karran S. , Smythe Patricia , Talbot S. , Turnell D. , Ørskov H. 
Published: August 2015

1. The mechanism of the purported protein-sparing effects of different postoperative intravenous regimens still remains controversial. We have therefore measured circulating concentrations of metabolites and hormones in blood and urine nitrogen excretion in patients receiving (a) sodium chloride solution (saline), (b) 1.5 g of glucose day−1 kg−1 body weight, (c) 1.5 g of glucose day−1 kg−1 with insulin (0.56 unit day−1 kg−1) or (d) mixed amino acids (1.5 g day−1 kg−1) after abdominal operation.
2. Compared with results for saline-treated patients, glucose infusion resulted in raised glucose and insulin concentrations and lowered ketone body and non-esterified fatty acid concentrations but did not influence protein catabolism.
3. Addition of insulin lowered blood glucose by approximately 1 mmol/l. Total nitrogen excretion during glucose/insulin infusion was significantly less than during saline infusion.
4. Infusion of amino acids, compared with saline infusion, resulted in raised blood glucose, alanine, serum insulin and plasma glucagon concentrations but lower concentrations of plasma non-esterified fatty acids and blood ketone bodies. Insulin concentrations, however, were similar in both amino acid- and glucose-treated groups.
5. Amino acid infusion increased urea and total nitrogen excretion but net nitrogen loss was only 1.9 mmol of nitrogen day−1 kg−1 compared with 12.7 mmol day−1 kg−1 in the saline-treated group and 11.0 mmol day−1 kg−1 in the glucose-treated group.
6. Glucose (and insulin) infusion appeared to inhibit gluconeogenesis, and amino acids to enhance it. The nitrogen-sparing effect of amino acids appears largely related to their mass and is apparently unrelated to changes in ketone bodies and insulin.
Subcellular Fractionation Studies on Hepatic Tissue from a Patient with Pompe's Disease (Type II Glycogen-Storage Disease)
Authors: Peters T. J. , Jenkins W. , Dubowitz V. 
Published: August 2015

1. An homogenate of liver biopsy taken from a patient with Pompe's disease (type II glycogen-storage disease) was analysed by enzyme microassay and subcellular fractionation by sucrose-density-gradient centrifugation.
2. A strikingly low activity of lysosomal acid α-d-glucosidase was noted but there was also increased activity of neutral α-d-glucosidase (found in endoplasmic reticulum).
3. Activities of the acid hydrolases, acid phosphatase and β-N-acetyl-d-glucosaminidase, were elevated compared with those of controls. Measurement of latent β-N-acetyl-d-glucosaminidase activity and results of subcellular fractionation experiments, indicated a marked fragility of certain populations of lysosomes. Lysosomes containing predominantly acid phosphatase and β-d-glucuronidase activities appeared to have normal integrity.
4. Assessment of organelle pathology by enzyme microassay indicated low mitochondrial and peroxisomal enzyme activities. In addition there was evidence of mitochondrial damage as reflected by increased sucrose permeability and by ultrastructural studies.
Prostaglandin Synthesis and Inactivation in Kidneys and Lungs of Rats with Experimental Diabetes
Authors: Hoult J. R. S. , Moore P. K. 
Published: August 2015

1. Microsomal prostaglandin synthesis and tissue prostaglandin concentrations in the kidneys of rats made diabetic by pretreatment with alloxan or streptozotocin were significantly decreased but were unchanged in lungs.
2. Prostaglandin inactivation was increased in kidneys of alloxan-diabetic rats but not changed in streptozotocin-diabetic kidneys or in the lungs of either group.
3. These changes in prostaglandin metabolism may cause a renal prostaglandin deficit and could contribute to certain pathological sequelae observed in diabetes mellitus.
The Effects of Treatment with Insulin on Serum High-Density-Lipoprotein Cholesterol in Rats with Streptozotocin-Induced Diabetes
Authors: Durrington P. N. , Stephens W. P. 
Published: August 2015

1. No significant difference in serum high-density-lipoprotein (HDL) cholesterol was observed when control rats were compared with rats with streptozotocin-induced diabetes of 14 days duration. Blood glucose and serum cholesterol and triglyceride concentrations were significantly higher in the diabetic group.
2. In a second experiment rats with streptozotocin-induced diabetes of 8 days duration were given long-acting porcine insulin (1 unit/day or 3 units/day subcutaneously for 14 days) and were compared with a control group. Blood glucose and serum cholesterol and triglyceride concentrations did not differ significantly with the two doses of insulin and there was no significant difference between serum high-density-lipoprotein cholesterol in control rats and either of the two groups of rats given insulin.
3. When the rats given insulin were grouped according to their blood glucose concentrations, those with blood glucose in the range 20–30 mmol/l were found to have significantly higher serum high-density-lipoprotein cholesterol concentrations than those with higher or lower blood glucose levels or than controls. There was thus a statistically significant curvilinear relationship between blood glucose and serum high-density-lipoprotein cholesterol concentrations.