bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Study of Changes in Whole-Body Calcium, Phosphorus, Sodium and Nitrogen by Neutron Activation Analysis in Vivo in Rats on a Calcium-Deficient Diet
Authors: Boddy K. , Lindsay R. , Holloway I. , Smith D. A. S. , Elliott A. , Robertson I. , Glaros D. 
Published: August 2015

1. A method of measuring changes in the total body content of calcium, phosphorus, nitrogen and sodium in rats by activation analysis in vivo is described.
2. The change in the body content of the elements has been measured in rats on a calcium-deficient diet and in control animals, the body nitrogen being used to represent lean body mass for normalization.
3. There were significant differences in Ca/N and P/N but not in Ca/P ratios between the animals on a deficient diet and control animals at the end of the dietary period.
Neural Factors Contributing to Renin Release during Reduction in Renal Perfusion Pressure and Blood flow in Cats
Authors: Stella A. , Calaresu F. , Zanchetti A. 
Published: August 2015

1. The participation of neural mechanisms in mediating the renin release induced by reduction of renal perfusion pressure was explored in anaesthetized cats by comparing renin release from the two kidneys, one acutely denervated and the other intact.
2. Suprarenal aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and halved blood flow to both kidneys, but caused a greater release of renin from the innervated kidney than from the contralateral denervated one (increments of 72 ± 17 and 29 ± 20 pmol/min respectively).
3. A study of the time-course of the response during aortic stenosis of 30 min duration showed early release of renin from the innervated kidney at a time (5 min) when little release occurred from the denervated one. In later samplings (15 and 30 min) the response of the innervated kidney levelled out at somewhat lower values, and that of the denervated organ progressively increased, but remained smaller than on the side with intact nerves.
4. There was no parallelism between renin release and renal vasomotor changes induced by aortic stenosis, as vasomotor changes were equal in the two kidneys and remained constant from beginning to end of stenosis. It is concluded that a significant part of the renin release induced by aortic stenosis is dependent on neural mechanisms: the neural differs from the non-neural component in being of more rapid onset and probably of shorter duration.
Vasopressin and Malignant Deoxycorticosterone Hypertension in Rats
Authors: Möhring J. , Möhring B. , Petri M. , Haack D. 
Published: August 2015

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated.
2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality.
3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure.
4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure.
5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin—angiotensin system plays in the pathogenesis of malignant renal hypertension.
Renal Hypertrophy in Streptozotocin-Diabetic Rats
Authors: Seyer-Hansen K. 
Published: August 2015

1. Kidney weight and content of protein, RNA and DNA were measured in rats with streptozotocin diabetes of varying duration.
2. Diabetic rats had larger kidneys than control rats: after 3 days of diabetes the weight increase was 15% and after 42 days of diabetes it was 90%. The protein content rose in parallel to the weight.
3. RNA content was already increased after 36 h of glycosuria, whereas DNA content was unchanged for the first 3 days of diabetes, and increased thereafter. The protein/DNA ratio increased rapidly during the first 3 days but remained constant thereafter.
4. Insulin treatment decreased the renal weight gain by about 67% during the first 8 days of diabetes, but did not prevent the increase in DNA. When insulin was started after 25 days of diabetes there was only a slight regression of kidney growth.
Regulation of Breathing during Exercise in Normal Subjects and in Chronic Lung Disease
Authors: Bradley G. W. , Crawford R. 
Published: August 2015

1. The breathing pattern in normal subjects during exercise was compared with that in patients with obstructive and restrictive lung defects.
2. In most normal women and patients with obstructive or restrictive lung disease, as the frequency of breathing increased both inspiratory and expiratory duration fell. However, in most normal men (74%) inspiratory duration did not fall as ventilation increased.
3. Women breathed faster than men, and both obstructed and restricted patients breathed faster than normal subjects.
4. The airflow patterns in normal men and women were similar, but most patients with restrictive or obstructive lung disease showed an approximately exponential fall in flow during expiration.
Self-Paced Walking as a Method for Exercise Testing in Elderly and Young Men
Authors: Bassey E. Joan , Fentem P. H. , MacDonald I. C. , Scriven Patricia M. 
Published: August 2015

1. An exercise test has been developed which is suitable for elderly or frail subjects. It is based on free walking at three different speeds on a level indoor course of 256 m. The subject sets his own pace in accord with simple instructions.
2. Twenty-four elderly men and ten young men took part in the study.
3. The time and number of paces taken to cover two sections of 100 m within the course were used to establish that the subjects walked steadily. Walking speed, pace frequency and stride length were then calculated.
4. Heart rate was obtained with body-borne tape recorders and related to the walking speed. The heart rate at a standard walking speed could then be obtained by interpolation. This is an assessment of the cardiovascular response to exercise (physical condition). The variation on repeating the test was ±5% and there was no significant difference between the two age groups.
5. The assessment was found to correlate moderately well with a conventional assessment of physical condition based on oxygen uptake from tests on a bicycle ergometer.
6. The test could also be used as a performance index since walking speed was characteristic for the subject. The younger group walked significantly faster than the older group. As a performance index the test is therefore sensitive to age differences.
Effects of Blood Pressure Reduction on the Structural Vascular Abnormality in Skin and Muscle Vascular Beds in Human Essential Hypertension
Authors: Sivertsson R. , Hansson L. 
Published: August 2015

1. Vascular resistance at maximal vasodilatation was examined in two vascular beds in two groups of hypertensive patients and in normotensive control subjects before and during anti-hypertensive therapy in the hypertension groups.
2. In one group of twelve untreated patients with essential hypertension, examined with plethysmography and intra-arterial blood pressure recording, a significantly higher vascular resistance at maximal vasodilatation was found in the hands compared with normotensive control subjects matched for age, sex, weight and height. This indicated a structural vascular abnormality in the patient group.
3. After 5 years of anti-hypertensive therapy in the patient group the difference in vascular resistance between patients and control subjects had decreased significantly, indicating a reversibility of the structural vascular abnormality.
4. Vascular resistance at maximal vasodilatation was examined in the calves of twelve untreated patients with essential hypertension and fourteen normotensive control subjects. Plethysmographic technique and indirect blood pressure recordings were used. A significantly higher vascular resistance was found in patients than in control subjects, indicating a structural vascular abnormality also in this vascular bed.
5. Anti-hypertensive treatment for 6 months in the patient group did not change vascular resistance at maximal dilatation, indicating that the structural vascular abnormality remained.
6. During acute reduction of blood pressure in hypertension by means of trimethaphan infusion, blood pressure and blood flow to the hands were reduced proportionally with no change of vascular resistance at maximal vasodilatation.
7. This indicates that resistance at maximal dilatation was unaffected by the acute reduction of blood pressure, in contrast to the findings after prolonged reduction of blood pressure in this vascular bed.
Ventricular Performance after Onset of Renal Hypertension
Authors: Ferrario C. M. , Kosoglov A. , Bajbus R. , Nadzam G. R. 
Published: August 2015

1. In renal hypertensive dogs, the slope of the relation between either stroke volume or cardiac output and end-diastolic pressure is shifted to the right of the normal curves.
2. The maximum to which stroke volume or cardiac output can be raised during loading is significantly less. These changes in cardiac performance appear to be unrelated to the severity of hypertension.
Evidence against Inhibition of the Renin—Angiotensinogen Reaction by Des-Angiotensin Substrate in the Rat
Authors: Hackenthal E. , Hackenthal R. , Hofbauer K. G. 
Published: August 2015

1. The possible inhibitory effect of des-angiotensin I substrate on the renin-substrate reaction was studied. For this purpose rat angiotensinogen was purified 50-fold from plasma of nephrectomized rats. Des-angiotensin substrate was prepared from the purified angiotensinogen preparation by reaction with immobilized hog renin (coupled to Sepharose).
2. In kinetic experiments it was found that des-angiotensin I substrate in concentrations of 0·225 and 0·45 μmol/l has no influence on the reaction between rat renin and rat angiotensinogen.
High-Renin Essential Hypertension: Adrenergic Cardiovascular Correlates
Authors: Esler M. , Julius S. , Randall O. , Dequattro V. , Zweifler A. 
Published: August 2015

1. Patients with mild essential hypertension and elevated plasma renin activity, when compared with normal subjects and hypertensive subjects with normal plasma renin, demonstrated features of sympathetic nervous cardiovascular excitation, accompanied by a raised plasma noradrenaline concentration.
2. An elevated heart rate at rest, shortened cardiac pre-ejection period, and greater heart rate reduction with acute β-adrenoreceptor blockade (intravenous propranolol) in high-renin essential hypertension were indicative of adrenergic cardiac excitation. An elevated total peripheral vascular resistance at rest and a greater fall in peripheral resistance with α-adrenoreceptor blockade (intravenous phentolamine) suggested the existence of a neurogenic increase in arteriolar resistance.
3. Blood pressure was normalized by ‘total’ autonomic blockade (atropine plus propranolol plus phentolamine) in the hypertensive subjects with elevated plasma renin activity.
4. These findings suggest that in mild high-renin essential hypertension increased adrenergic drive to the heart and resistance vessels exists. The elevation of blood pressure is sustained predominantly by neurogenic mechanisms. The high plasma renin activity is seen as an expression of sympathetic nervous system overactivity.
Change in the Renin Dependency of Blood Pressure Induced by Volume Depletion and/or Propranolol Therapy in Hypertensive Patients
Authors: Geyskes G. G. , Boer P. , Vos J. , Mees E. J. Dorhout 
Published: August 2015

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113).
2. The P113-induced fall of the blood pressure did correlate with the log PRA (r = 0·888, P < 0001). This correlation was found irrespective of different types of hypertension and treatment schedules.
3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency.
4. No indication was found that a given PRA is of special importance for blood pressure elevation in different patients.
5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.
Significance of Increase in Labelled Albumin Disappearance Rate in Arterial Hypertension
Authors: Ulrych M. , Ulrych Z. 
Published: August 2015

1. Relationships between labelled albumin disappearance rate (LADR), plasma volume, blood volume, plasma renin activity (PRA) and blood pressure (BP) were studied in normotensive control subjects and patients with hypertension of different aetiology and severity. In essential hypertensive patients without complications an inverse linear relationship was found between blood pressure and plasma or blood volume.
2. Very close inverse correlations were found between LADR and PRA in both normotensive subjects and patients with uncomplicated essential hypertension. LADR appears to be an excellent reference standard for PRA.
3. It is postulated that LADR mainly reflects the relation between circulating fluid and vascular capacitance tone. LADR is increased in hypertension and blood volume may still be inappropriately high.
Plasma Renin Concentration and the Hypotensive Effect of Bendrofluazide and of Atenolol
Authors: Fagard R. , Amery A. , Deplaen J. F. , Lijnen P. , Missotten A. 
Published: August 2015

1. The anti-hypertensive effect of atenolol was greater than that of bendrofluazide.
2. The change in systolic blood pressure caused by bendrofluazide showed a significant inverse correlation with the plasma renin concentration (r = −0·47; P < 0·01).
3. The correlation between the change in systolic blood pressure caused by atenolol and the plasma renin concentration was not significant (r = 0·28; 0·1 > P > 0·05).
4. Plasma renin concentration was unaffected by atenolol.
Results and Costs of Investigating Newly Detected Hypertensive Patients
Authors: Smith E. K. M. , Viol G. W. , Toi A. 
Published: August 2015

1. Eighty unselected hypertensive subjects were investigated at a cost of $78.00 per patient, in a short out-patient study programme. Seven (9%) were found to have a cause for their hypertension; incidental abnormalities were found in twenty-two (28%).
2. The combination of clinical selection and planned out-patient investigation should detect all patients with secondary hypertension.
Effects of Indomethacin in Rabbit Renovascular Hypertension
Authors: Strong C. G. , Romero J. C. 
Published: August 2015

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension.
2. Ten intravenous inject ons (3 mg day—1 kg—1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), and ten rabbits with one-kidney Goldblatt hypertension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay.
3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1·15 to 0·2 ng/ml, sem 0·2; P < 0·01) and plasma renin activity (20 to 3 ng h—1 ml—1, sem 1, P < 0·01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin.
4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31·5 ng h—1 ml—1, sem 3 and 4 respectively; P < 0·01) and plasma prostaglandin E2 (1·2 to 3·4 ng/ml, sem 0·2 and 0·4 respectively; P < 0·05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7·6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, sem 7·7) and death within 5 days.
5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, sem 4 and 6 respectively; P < 0·01) and decreased renal function (plasma creatinine 0·9 ± 0·04 to 3·5 ± 1 mg/100 ml, sem 0·04 and 1 respectively; P < 0·01).
6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities.
7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
Renal Prostaglandin Synthesis in Hypertension Induced by Deoxycorticosterone and Sodium Chloride in the Rat
Authors: Pugsley D. J. , Mullins Rachel , Beilin L. J. 
Published: August 2015

1. The role of renal medullary prostaglandin E has been examined in rats with hypertension induced by sodium chloride and deoxycorticosterone (salt—DOC).
2. Synthesis of prostaglandin E was normal in early salt—DOC hypertension. Indomethcin exacerbated the hypertension, and depressed synthesis of prostaglandin E equally in hypertensive and control rats.
3. Synthesis of prostaglandin E was depressed in rats with late salt—DOC hypertension.
4. The results lend support to the concept that prostaglandin E is involved in the regulation of arterial pressure.
Effects of Stimulation and Inhibition of the Renal Prostaglandin Synthetase System on Renin Release in vivo and in vitro
Authors: Weber P. C. , Larsson C. , Hamberg M. , Änggård E. , Corey E. J. , Samuelsson B. 
Published: August 2015

1. The prostaglandin precursor arachidonic acid (C20:4) increases plasma renin activity in the rabbit and rat when it is infused into the renal arteries.
2. The increase in plasma renin activity after C20:4 in rats is not changed by volume expansion.
3. The inhibitor of prostaglandin synthesis indomethacin decreases plasma renin activity in the rabbit.
4. The increase in plasma renin activity after total renal ischaemia is abolished by pretreatment with indomethacin.
5. C20:4 increases dose- and time-dependent renin release from slices of rabbit kidney cortex.
6. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment in vivo, and addition to the incubation medium, reduces basal as well as C20:4-stimulated renin release in vitro.
7. The stimulating effect of C20:4 on renin release is assumed to be caused directly by formation of prostaglandin endoperoxides in the kidney cortex and not by prostaglandins since in vitro a natural prostaglandin endoperoxide (PGG2) and two stable synthetic prostaglandin endoperoxide analogues (EPA I and EPA II) do increase the release of renin, but PGE2 has no effect and PGF2α inhibits renin release.
The Effects of Aldosterone and Spironolactone on Renal Kallikrein in the Rat
Authors: Margolius H. S. , Chao Julie , Kaizu T. 
Published: August 2015

1. A technique has been developed for the measurement of kallikrein ‘production’ in rat renal cortical cells in suspension.
2. After preparative steps, column chromatography on DEAE-cellulose yielded a peak of α-N-tosyl-l-arginine methyl ester (Tos-Arg-OMe) esterase activity identical with kallikrein isolated from rat urine in respect of pH optimum, effects of inhibitors, biological activity and immunological properties.
3. The nutrient medium surrounding incubated cells contained measurable kallikrein activity, which was increased by aldosterone and decreased by spironolactone.
4. The results raised the possibility that kallikrein could be an aldosterone-induced protein.
Further Unravelling of the Causes of ACTH-induced Hypertension in the Sheep
Authors: Coghlan J. P. , Denton D. A. , Fan J. S. K. , McDougall J. G. , Scoggins B. A. , Shulkes A. A. 
Published: August 2015

1. Acute severe sodium subtraction (20–25% of total exchangeable sodium) before or during treatment with adrenocorticotrophic hormone (ACTH) does little to modify the increase in blood pressure induced by ACTH.
2. Chronic low salt diet, less than 5 mmol/day, abolishes the blood pressure increase, but the response can be restored by increasing the sodium intake to as little as 10 mmol/day.
3. 17α,20α-Dihydroxyprogesterone infused concurrently with other adrenal steroids will mimic ACTH hypertension and perhaps represents a new class of steroid capable of influencing btood pressure.
Influence of Spironolactone on Endogenous Steroid Metabolism in Man
Authors: Abshagen U. , Spörl S. , Schöneshöfer M. , L'Age M. , Rennekamp H. , Oelkers W. 
Published: August 2015

1. Mild secondary hyperaldosteronism was induced in ten healthy young males by a low sodium diet for 14 days. After 7 days on the diet, five subjects each were treated with spironolactone (group S) or triamterene (group T) daily.
2. The daily negative sodium balance was identical during the first 3 days of medication with both drugs but sodium loss was more severe during the following days in group S. Consequently, the plasma renin activity was higher during the last days of spironolactone compared with triamterene medication.
3. Changes in plasma electrolytes were similar in both groups.
4. No influence of either drug on the synthesis chain leading to Cortisol was observed.
5. Plasma concentrations of deoxycorticosterone and corticosterone, however, increased considerably in group S, whereas triamterene did not influence these steroids.
6. Whereas triamterene induced a prompt increase of plasma aldosterone, an increase was delayed for the first 3 days of treatment with spironolactone. Later, plasma aldosterone concentrations rose rapidly in group S and were no longer different from those in group T.
7. Results are interpreted as being due to an initial inhibition of aldosterone synthesis by spironolactone, which is finally compensated, at least in part, by increased activation of the renin-angiotensin system.
The Role of 11-Deoxycorticosterone in Human Hypertension
Authors: Tan S. Y. , Noth R. H. , Mulrow P. J. 
Published: August 2015

1. Using a newly developed and validated radio-assay method, we have measured plasma 11-deoxycorticosterone concentrations in a wide spectrum of human hypertensive states.
2. Patients with essential and renovascular hypertension have normal plasma concentrations of 11-deoxycorticosterone.
3. Elevated concentrations are seen in some patients with primary aldosteronism, Cushing's syndrome, low-renin hypertension, and in adult hypertensive subjects with elevated urinary 17-ketosteroid excretion.
4. An aetiological role for deoxycorticosterone in certain forms of human hypertension appears likely.
Brain-Stem Structures and Catecholamines in the Control of Arterial Blood Pressure in the Rat
Authors: De Jong W. , Zandberg P. , Versteeg D. H. G. , Palkovits M. 
Published: August 2015

1. Noradrenaline, adrenaline and α-methylnoradrenaline administration into the nucleus tractus solitarii (NTS) of anaesthetized rats decreased blood pressure and heart rate in a dose-dependent fashion.
2. Bilateral injections were effective in lower doses than unilateral administration. α-Methylnoradrenaline given bilaterally produced hypotension in a dose of 0·08 nmol whereas after unilateral injection a dose of 0·32 nmol was needed to obtain the same degree of hypotension.
3. Electrical stimulation of the NTS caused hypotension and bradycardia. Conversely, bilateral electrolytic lesions or deafferentation of the NTS led to acute hypertension. Chronically such lesions caused neurogenic hypertension.
4. In spontaneously hypertensive rats increased concentrations of noradrenaline, adrenaline and dopamine were measured in the part of the NTS located just caudal to the obex (A2 region).