bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of 47Ca Kinetics in Normal Subjects by Means of a Compartmental Model with a Non-Exchangeable Plasma Calcium Fraction
Authors: Wajchenberg B. L. , Leme P. R. , Ferreira M. N. L. , Filho J. Modesto , Pieroni R. R. , Berman M. 
Published: August 2015

1. 47Ca kinetic studies were performed in eight normal young adult males. Plasma, urinary and faecal stable and radioactive calcium and whole-body radioactivity were measured for up to 40 days after intravenous administration of the tracer.
2. The plasma radioactivity data could be fitted to the sum of four exponentials corresponding to a four-compartment model, but this model did not account for the consistently greater 47Ca specific radioactivities in plasma relative to those in urine at the same time in five of the subjects.
3. A non-exchangeable fraction of plasma calcium estimated as 5% of the mass in the plasma compartment was postulated to account for this finding.
4. An estimate of the insensible losses of calcium was obtained from the whole-body radioactivity counting data.
Intestinal Transport of a Tetrapeptide, l-Leucylglycylglycylglycine, in Rat Small Intestine in Vivo
Authors: Chung Y. C. , Silk D. B. A. , Kim Y. S. 
Published: August 2015

1. The intestinal transport mechanism for the tetrapeptide l-leucylglycylglycylglycine, Leu-Gly-Gly-Gly, and its relation to the transport of free Leu, Leu-Gly and Leu-Gly-Gly were investigated in vivo by means of jejunal perfusion in rats.
2. The rates of net Leu absorption from peptides (Leu-Gly and Leu-Gly-Gly-Gly) were significantly greater than those from the free amino acid mixtures when the test solutions were perfused at a concentration of 15 mmol/l.
3. Net Leu absorption rates from Leu-Gly (10 μmol/ml) and Leu-Gly-Gly (10 μmol/ml) were extensively inhibited (84% and 68% respectively) by Gly-Pro at 100 mmol/l, whereas Gly-Pro had no effect on Leu absorption from Leu-Gly-Gly-Gly. l-Alanine (Ala, 100 μmol/ml), on the other hand, which completely inhibited Leu absorption during perfusion of free Leu, inhibited Leu uptake from Leu-Gly-Gly-Gly only about 50% at all concentrations studied. Ala had no effect on Leu absorption from Leu-Gly and Leu-Gly-Gly (10 μmol/ml).
4. Neither Ala at 100 μmol/ml nor Gly-Pro at 100 μmol/ml had any effect on brush-border aminopeptidase activity in vitro, suggesting that the hydrolytic capacity of the intestinal mucosal brush border was unaltered when Ala or Gly-Pro was included in the perfusion mixture. l-Alanyl-β-naphthylamide (20 μmol/ml), which inhibited brush-border aminopeptidase activity by 85% in vitro, failed to block substantially net Leu absorption from Leu-Gly and Leu-Gly-Gly-Gly.
5. The data presented suggest that, although some of the Leu from the tetrapeptide, Leu-Gly-Gly-Gly, may be hydrolysed before transport, nearly 50% of the tetrapeptide appears to be transported intact. Although Leu-Gly, Leu-Gly-Gly and Gly-Pro seem to share a common transport mechanism, the system used for intact Leu-Gly-Gly-Gly absorption seems to be distinct. However, the present study does not exclude the possibility that binding of the tetrapeptide to the brush-border aminopeptidase alters the affinity of Leu for the amino acid carrier, and therefore further studies are necessary before firm conclusions can be made on the general mechanism of tetrapeptide transport.
Evidence that the Acute Cardiovascular Response to Isoprenaline is Partly Mediated via Renin Release
Authors: Anderson G. H. 
Published: August 2015

1. The possible effect of the increased plasma renin activity induced by β−adrenoreceptor stimulation in supporting arterial pressure has been studied in five normal subjects on a diet of 100 mmol of sodium/day for 4 days or 40 mmol of sodium/day for 4 days by infusing isoprenaline at 1·0, 2·0 or 3·0 μg min−170 kg−1, each for 1 h with 45 min between each infusion rate. During the last 30 min of each isoprenaline dose, the angiotensin II analogue [Sar1, Ala8]angiotensin II (saralasin) was infused.
2. Isoprenaline significantly (at least P &lt;0·05) increased the pulse rate, systolic arterial pressure and plasma renin activity; the diastolic blood pressure decreased but the mean arterial pressure did not change. Saralasin administered to subjects on the 100 mmol of sodium/day diet significantly (at least P &lt; 0·05) lowered mean arterial pressure at the two highest isoprenaline infusion rates.
3. With patients on a low sodium diet, saralasin lowered mean arterial pressure at all three isoprenaline infusion rates. On the low sodium diet the fall in mean arterial pressure caused by saralasin was significantly greater (P &lt; 0·05) at the isoprenaline infusion rate of 3·0 μg min−1 70 kg−1 than at the infusion rate of 1·0 μg min−1 70 kg−1. The change in mean arterial pressure with saralasin before and during isoprenaline infusion on both diets was significantly correlated (r = −0·39, n = 38, P &lt; 0·01) with the plasma renin activity measured immediately before saralasin infusion.
4. It is concluded that during β−adrenoreceptor stimulation the increased plasma renin activity (acting through angiotensin) supports arterial pressure.
Measurement of Water Distribution and Transcapillary Solute Flux in Dog Lung by External Radioactivity Counting
Authors: Prichard J. S. , Lee G. de J. 
Published: August 2015

1. A method for measuring the pulmonary water compartments in vivo in anaesthetized dogs is described.
2. The technique depends upon the sequential intravenous injection of markers labelled with γ-ray-emitting isotopes. Each is allowed to become evenly distributed throughout the compartment to which it is confined. A calibrated γ-counter placed at the surface of the inflated lung then records a count rate related to the total quantity of isotope in unit volume of tissue. The size of each water compartment can be calculated from the external count rate and the isotopic concentration of the marker in plasma.
3. The markers used were 125I-labelled serum albumin for plasma, [125I]iodide for extracellular water and [125I]iodoantipyrine for total water.
4. The method was extended to calculate transcapillary flux rates of serum albumin and showed that rapid exchange of serum albumin takes place between the plasma and interstitial space.
5. Results obtained non-invasively by the isotopic method were compared with direct measurements. Agreement was good.
Effect of Chronic Clonidine Treatment and its Abrupt Cessation on Mean Blood Pressure of Rats with a Normal or An Elevated Blood Pressure
Authors: Atkinson J. , Boillat Nicole , Pera-Bally Roselyne , Peters-Haefeli Lise , Kirchertz E. J. 
Published: August 2015

1. Clonidine (6 mg of base/1 of water) was given as drinking fluid to normotensive rats or rats with established or early hypertension.
2. Spontaneous hypertensive rats (6 months old: average dose of clonidine, 0·6 mg 24 h−1 kg−1) showed a sustained fall in blood pressure over 3 weeks.
3. The same clonidine solution given for 6 weeks to two-kidney Goldblatt rats with early-stage hypertension (average dose of clonidine: 1 mg 24 h−1 kg−1) or spontaneously hypertensive rats (clonidine dose: 1 mg) induced a fall in mean blood pressure, but no change in normotensive rats.
4. Replacement of clonidine by water induced hypertension and lability which led to death in hypertensive but not in normotensive rats.
Cardiovascular Design after ‘Reversal’ of Long-Standing Renal Hypertension in Rats
Authors: Lundgren Y. , Weiss Lilian 
Published: August 2015

1. After 4–5 months of renal hypertension in rats renal artery ‘declipping’ was performed. Eight weeks afterwards paired hindquarter perfusions were performed on the declipped rats and normotensive control rats, exploring the relationships between mean arterial pressure and flow, from maximal vasodilatation to maximal vasoconstriction, induced by graded noradrenaline infusions. Left ventricular weights were measured.
2. Declipping caused a fall in mean arterial pressure from 180 to 135 mmHg, though still after 8 weeks the mean pressure was 19% higher than in normotensive control rats.
3. All parameters reflecting design and reactivity of the resistance vessels and left ventricular weight decreased significantly, but not as much as mean arterial pressure, and were still significantly increased compared with those of control rats.
4. Thus neither mean arterial pressure nor cardiovascular design was normalized 8 weeks after ‘reversal’ of long-standing renal hypertension, in contrast to short-standing renal hypertension where both are completely normalized 3 weeks after declipping.
Effect of Acid, Trypsin and Cold Treatment and of Renin— Plasma Interaction on the Activity of Renin Secreted by Rat Kidney
Authors: Nakane H. , Nakane Y. , Corvol P. , Menard J. 
Published: August 2015

1. Renin release from the isolated perfused rat kidney was markedly stimulated by isoprenaline or anoxia. Renin secreted into the blood-free perfusate was not activated by exposure to cold or dialysis to pH 3·3, suggesting the absence either of cryo- or acid-activatable renin or of factors necessary to activate inactive renin.
2. Trypsin treatment did not change renin concentration in the perfusate samples.
3. When binephrectomized rat plasma was added to perfusate samples before dialysis, renin concentration in the acidified samples was significantly higher than in samples dialysed to pH 6·5. Diminished renin recovery in the latter samples caused this difference. Binephrectomized rat plasma itself had no significant renin activity before or after acid dialysis, indicating the absence of any important extrarenal source of active or acid-activatable renin in rats.
4. Acidification of binephrectomized rat plasma before its addition to the perfusate samples markedly reduced the difference between renin recovery during dialysis to pH 3·3 and dialysis to pH 6·5, indicating that acidification irreversibly inhibited renin inactivation by binephrectomized rat plasma. No net increase in renin concentration was observed in any of our experiments.
5. These results suggest that rat kidney does not secrete inactive renin. They also point to the existence of renin inactivation by rat plasma at neutral pH, which might lead to overestimation of acid-activatable renin in rats.
Choice of Control Groups in the Appraisal of Sympathetic Nervous Activity in Essential Hypertension
Authors: Jones D. H. , Hamilton Carlene A. , Reid J. L. 
Published: August 2015

1. Plasma noradrenaline concentrations were similar in normotensive and hypertensive outpatients, but were significantly lower in laboratory control subjects.
2. Standing plasma noradrenaline concentrations were similar in all three groups.
3. Urinary vanillyl mandelic acid, catecholamines and metanephrines were also similar in the normotensive and hypertensive groups.
4. Laboratory controls, possibly because of familiarity with the techniques of sphygmomanometry and blood sampling, may attain a ‘basal’ resting level of sympathetic nervous discharge more readily and rapidly than subjects who are unfamiliar with such procedures.
5. After orthostatic stimulation by standing for 2 min, the activity of the sympathetic nervous system, as determined by pulse rate and plasma noradrenaline concentrations, was similar in the three groups, despite the lower starting values in the laboratory staff.
6. The absence of differences in plasma noradrenaline or urinary catecholamine and metabolite concentrations does not support the hypothesis of excessive sympathetic nervous activity in essential hypertension.
Effect of Propranolol on the Ventilatory Response to Hypercapnia in Man
Authors: Trembath P. W. , Taylor Elizabeth A. , Varley J. , Turner P. 
Published: August 2015

1. The effect of a single oral dose of propranolol on the ventilatory response to hypercapnia has been studied in five healthy subjects.
2. Propranolol produced a small but significant reduction in the slope of the ventilation/end-tidal Pco2 regression line.
3. Propranolol did not significantly change vital capacity or forced expiratory volume in 1 s.
Effect of General Anaesthesia on Renal Haemodynamics in the Rat
Authors: Koeppen B. M. , Katz A. I. , Lindheimer M. D. 
Published: August 2015

1. The effect of sodium pentobarbital and Inactin anaesthesia on renal haemodynamics in the rat was evaluated with radioactive microspheres 15 μm in diameter.
2. Both anaesthetic agents caused substantial decrements in total renal blood flow (sodium pentobarbital, −34%; Inactin, −24%) compared with unanaesthetized animals.
3. Measurements of renal function obtained in rats anaesthetized with either of these anaesthetic agents should be interpreted with caution.
Impairment of Flow in Routine Gravity-Fed Intravenous Infusions to Surgical Patients
Authors: Clarke E. W. , Jamison J. P. , Quartey-Papafio J. B. 
Published: August 2015

1. Gravity-fed intravenous infusions were studied in patients by using continuous flow recording and a new resistance-measuring method.
2. A common, though preventable, cause of reduced flow was the gradual deformation of the plastic tubing under the regulator clamp.
3. In many cases there was some constriction of the cannulated vein and in a few this constriction was severe enough to seriously impair the infusion. The severity of the constriction varied periodically.
4. There was no evidence of trouble due to a generally raised pressure in the arm veins nor was clotting in the cannula a serious problem.
5. A simple test is described which may be found useful clinically for assessing the difficult infusion.
Vascular Reactivity in the Pathogenesis of Spontaneous Hypertension
Authors: Berecek Kathleen H. , Rascher W. , Gross F. 
Published: August 2015

1. Alterations in vascular reactivity were assessed in isolated artificially perfused kidneys from stroke-prone spontaneously hypertensive (spSH) rats at different stages of hypertension and after neonatal sympathectomy with 6-hydroxydopamine (6-OHDA).
2. During the pre-hypertensive stage, and the early and chronic stages of hypertension, the responses to noradrenaline, vasopressin, serotonin and angiotensin II were enhanced in renal vascular beds from spSH animals compared with age- and sex-matched Wistar—Kyoto (WK) rats; dose—response curves were shifted to the left, had steeper slopes, greater maximal responses and decreased thresholds.
3. With increasing severity and duration of hypertension, renal vascular resistance at maximal vasodilatation increased, the slopes of the dose-response curves were steeper and maximal responses were greater.
4. Neonatal sympathectomy with 6-OHDA greatly attenuated but did not prevent the eventual development of hypertension; furthermore, this treatment had no effect on the enhanced resistance or reactivity in renal vascular beds from spSH rats.
5. The appearance of enhanced resistance and reactivity in the early stages of hypertension and the inability to prevent these vascular changes by neonatal sympathectomy suggest that these alterations are a primary pathogenic mechanism in spSH rats.
Activators of Inactive Renin (‘Prorenin’) in Human Plasma: Their Connection with Kinin Formation, Coagulation and Fibrinolysis
Authors: Derkx F. H. M. , Bouma B. N. , Tan-Tjiong H. L. , Schalekamp M. A. D. H. 
Published: August 2015

1. Human plasma was treated at 4°C with acid, trypsin, plasmin, streptokinase, urokinase, active Hageman factor fragment (β-XIIa) and β-XIIa-activated plasma prekallikrein (Fletcher factor). The conversion of inactive into active renin (activation) was studied in normal plasma (n = 10), Hageman factor-deficient plasma (n = 2), Fletcher factor-deficient plasma (n = 1) and plasminogen-free plasma (n = 4).
2. In normal plasma inactive renin was activated at pH 7·5 after treatment at pH &lt; 4·0; at pH 3·3 the results were the same as with trypsin. This was also the case in plasminogen-free plasma. In Hageman factor-deficient plasma and in Fletcher factor-deficient plasma, however, the quantities of renin that were activated after acidification were much smaller than with trypsin. The addition of physiological amounts of active kallikrein to pH 3·3-pretreated Hageman factor-deficient plasma caused complete activation of renin. In contrast, the addition of active Hageman factor fragment to pH 3·3-pretreated Fletcher factor-deficient plasma had little or no effect.
3. Plasmin, streptokinase-activated plasminogen and urokinase-activated plasminogen activated inactive renin in pH 4·0-pretreated normal plasma as well as in pH 4·0-pretreated Hageman factor-deficient plasma and Fletcher factor-deficient plasma.
4. It is concluded that inactive renin is activated by two separate proteolytic pathways: one pathway depends on both Hageman factor and plasma prekallikrein, and the other pathway depends on plasminogen. In the Hageman factor-dependent pathway plasma kallikrein and not Hageman factor is the major activator of inactive renin. It is assumed that pH 3·3-treatment of plasma destroys the major inhibitors of kallikrein and that pH 4·0-treatment destroys the major inhibitor of plasmin.
Plasmin Can Activate Plasma Prorenin but is Not Required for the Alkaline Phase of Acid Activation
Authors: Sealey Jean E. , Atlas S. A. , Laragh J. H. , Silverberg M. , Kaplan A.P. 
Published: August 2015

1. Plasma prorenin is an inactive form of renin that is converted into active renin at alkaline pH in previously acidified plasma; this conversion of prorenin into renin is mediated by Hageman factor-dependent activation of prekallikrein, which, in turn, leads to prorenin activation.
2. Since plasma kallikrein can activate plasminogen, the present studies were designed to evaluate whether alkaline-phase activation of prorenin by plasma kallikrein is mediated via plasminogen activation.
3. We demonstrated that plasminogen is present in acid-treated plasma in sufficient quantity to convert prorenin into renin after activation by streptokinase.
4. However, alkaline-phase activation was completely normal in plasminogen-free plasma.
5. Therefore alkaline-phase activation of plasma prorenin is mediated by plasma kallikrein but is not dependent on kallikrein activation of plasminogen.
Release of Active and Inactive Renin by the Human Kidney
Authors: Aoi W. , Seto S. , Doi Y. , Murayama M. , Tasaki S. , Suzuki S. , Kuramochi M. , Hashiba K. 
Published: August 2015

1. Active and inactive renin were assayed in plasma of the renal veins and the inferior vena cava below the kidney in eight patients with hypertension and unilateral renal abnormalities, 20 min after the patients had resumed the upright position.
2. The concentration of active renin on the affected side was significantly higher than that on the non-affected side. The concentration of inactive renin on the affected side was significantly lower than that on the non-affected side and in the inferior vena cava.
3. These findings suggest either that the affected kidney mainly secretes active renin, which is then converted into inactive renin in the extrarenal circulation, or that the affected kidney activates inactive renin.
Effect of Age on Angiotensin II Receptors from Rat Brain
Authors: Baxter Claire , Horvath J. , Duggin G. , Tiller D. 
Published: August 2015

1. Angiotensin II receptor binding was studied in specific regions of rat brain at different ages from birth to 14 weeks.
2. The number of specific angiotensin II receptors increased in all regions during the first 2 weeks of life and then decreased to adult levels. Peak numbers of receptors were up to 10 times the adult numbers.
3. The midbrain and thalamus-hypothalamus had maximum numbers of angiotensin II receptors at 2 weeks of age, whereas the rest of the brain regions had maximum numbers at 1 week.
4. Saralasin-infusion experiments suggested that circulating angiotensin-related peptides could reach brain angiotensin II receptors in 2 week old rats, but not in 6 week old rats.
5. It is postulated that the centrally mediated actions of circulating angiotensin II may be particularly important in the newborn.
Hormonal Changes with Long-Term Converting-Enzyme Inhibition by Captopril in Essential Hypertension
Authors: Matthews P. G. , McGrath B. P. , Johnston C. I. 
Published: August 2015

1. Captopril was shown to be as effective as hydrochlorothiazide in lowering the blood pressure in patients with moderately severe essential hypertension.
2. With the combination of captopril and hydrochlorothiazide satisfactory control of blood pressure was maintained over 8 months.
3. Inhibition of angiotensin converting enzyme by captopril in man was associated with falls in plasma angiotensin II and urinary aldosterone and rises in angiotensin I and plasma renin.
4. No change in venous concentrations of bradykinin could be demonstrated during therapy.
5. Captopril attenuated the hyperaldosteronism and hypokalaemia associated with diuretic therapy.
A Novel Orally Active Converting-Enzyme Inhibitor Ys 980: Effects on Blood Pressure in Spontaneously Hypertensive Rats
Authors: Unger Th. , Rockhold R. W. , Schaz K. , Vescei P. , Bönner G. , Rascher W. , Ganten D. 
Published: August 2015

1. The effects of long-term treatment with the angiotensin I converting-enzyme inhibitor YS 980 were examined in stroke-prone spontaneously hypertensive (sp-SH) rats. Development of hypertension was markedly blunted in the YS 980-treated animals.
2. Effective converting-enzyme inhibition was confirmed by significant increases in plasma angiotensin I (ANG I) and plasma renin concentration, inhibition of the pressor responses to intravenous ANG I and potentiation of the depressor responses to intravenous bradykinin.
3. Urinary free aldosterone excretion was decreased but no changes in urinary sodium and potassium excretion were observed.
4. The pressor responses to intravenous leucine-enkephalin were reduced.
5. The pressor responses to injection of ANG I and bradykinin into the lateral brain ventricle were unaltered.
6. We conclude that the antihypertensive action of YS 980 in sp-SH rats cannot be explained by the inhibition of the plasma renin-angiotensin system alone. Effects on other peptide systems must be considered.
α-Adrenergic Suppression of Renin Secretion in the Rat Independent of Renal Vasoconstriction
Authors: Vandongen R. , Strang K. D. , Poesse Marianne H. , Birkenhager W. H. 
Published: August 2015

1. The effect of α-adrenergic stimulation, with phenylephrine, on isoprenaline-provoked renin secretion was studied in the isolated perfused rat kidney.
2. Infusion of phenylephrine increased renal perfusion pressure and prevented renin secretion in response to isoprenaline.
3. Renal vasoconstriction was abolished and the response in renin secretion to isoprenaline was restored by α-adrenoreceptor blockade with phenoxybenzamine.
4. In contrast, when renal vasoconstriction was prevented by dihydrallazine, suppression of renin release by phenylephrine still occurred.
5. These observations support an inhibitory effect of a non-vascular α-adrenergic mechanism on renin release. It is suggested that the α-receptor mediating this effect is directly related to the renin-producing juxtaglomerular cell.