bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Autonomic Blockade on the Transient Changes in Cardiac Frequency on Relief of Hypoxia in Man
Authors: Petersen E. S. , Vejby-Christensen H. , Nielsen T. M. 
Published: August 2015

1. Acute hypocapnic hypoxia was induced in ten healthy subjects by the inhalation of O2+N2 (10:90) at rest and during exercise. Transient relief of hypoxia by two breaths of O2 (O2 test) resulted in a decrease in cardiac frequency which was highly significant about 10 s after the tests and never consistently delayed in comparison with the ventilatory changes.
2. β-Adrenergic blockade with propranolol reduced the magnitude of the changes in cardiac frequency but not their time-course.
3. Cholinergic blockade with atropine sulphate (and double blockade) abolished the early changes in cardiac frequency. During continued O2 breathing (3 min) small, still significant, changes were observed.
4. It is concluded that the decrease in cardiac frequency within 10 s of relief of hypoxia is dependent on efferent vagal activity.
The Effect of Glucose on the Urinary Excretion of Sodium and Hydrogen Ion in Man
Authors: Garnett E. S. , Nahmias C. 
Published: August 2015

1. Urinary sodium and hydrogen ion excretion was measured in four normal subjects before and after they had ingested 25 g of glucose. The subjects were studied during a sustained water diuresis after an overnight fast and after a 40 h fast.
2. After glucose had been ingested, urinary sodium excretion was reduced by approximately 40% but there was no change in urine flow. The decrease in sodium excretion was associated with a rise in hydrogen ion excretion.
3. These results suggest that sodium ion is retained in exchange for hydrogen ion in the distal segment of the nephron.
4. It is postulated that the increased renal bicarbonate threshold and the metabolic alkalosis which develop when glucose is given to fasted subjects are a consequence of this exchange.
Measurement of Deep Body Temperature from the Urine
Authors: Fox R. H. , Brooke O. G. , Collins J. C. , Bailey C. S. , Healey F. B. 
Published: August 2015

1. The relation between urine and rectal temperatures has been studied under a variety of conditions by using the Uritemp bottle, which measures deep body temperature from the urine.
2. This device gives a reliable measurement of deep body temperature and has advantages over both rectal and oral techniques for many clinical applications.
3. The development of a new and more reliable device, the Uritemp meter, is described. Urine is voided through a specially designed and disposable unit, equipped with either a standard mercury-in-glass thermometer or any one of a range of commercially available electronic thermometers. Provision is made to collect a urine sample simultaneously if required.
Changes in the Renin-Angiotensin-Aldosterone System and in Sodium and Potassium Balance during Development of Renal Hypertension in Rats
Authors: Leenen F. H. H. , Scheeren J. W. , Omylanowski D. , Elema J. D. , Van Der Wal B. , De Jong W. 
Published: August 2015

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160–180 mmHg; clip i.d. 0.25 mm) and severe (200–230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney.
2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160–180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred.
3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip.
4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.
The Distribution of Ammonia between Extracellular and Intracellular Compartments of the Rat Brain
Authors: Hindfelt B. 
Published: August 2015

1. The distribution of ammonia between extra- and intra-cellular compartments of the brain was evaluated in anaesthetized rats exposed to sustained hyperammonaemia and superimposed acute hypo- or hyper-capnia.
2. It is concluded that the concentration gradient for ammonia between arterial plasma and cerebrospinal fluid (CSF) cannot be explained by pH-dependent non-ionic diffusion of ammonia. A continuous uptake by the brain tissue of ammonia from the CSF is postulated and possible mechanisms are discussed.
Evidence for a Significant Contribution from Central Effects of Angiotensin in the Development of Acute Renal Hypertension in the Greyhound
Authors: Scroop G. C. , Katic F. P. , Brown M. J. , Cain M. D. , Zeegers P. J. 
Published: August 2015

1. The importance of central vasomotor effects of endogenously generated angiotensin in the acute hypertensive response to renal artery constriction has been investigated in the anaesthetized greyhound.
2. When the central cardiovascular action of angiotensin was abolished by thermocoagulation of the areas postrema, the hypertensive response to renal artery constriction was reduced by half while the increase in plasma renin activity was unchanged.
3. It is concluded that central vasomotor effects of angiotensin play a significant role in renin-dependent hypertension.
The response of the Renin-Angiotensin System in Rats to the Injection of Angiotensin II Antibodies
Authors: Hackenthal E. , Bauknecht H. , Oster P. 
Published: August 2015

1. Antibodies against angiotensin II were purified by affinity chromatography.
2. When injected intravenously into rats, the antibody distributed in the extracellular space with a half-time of 11 h and a distribution volume of about 10 ml/100 g body weight. The antibody was eliminated with a half-time of 7 days.
3. Plasma angiotensin II concentrations increased about 100-fold the control values 7 min after antibody injection and declined in parallel with the antibody concentration. It was calculated that only about 1–4% of the binding capacity of the antibody was occupied by angiotensin throughout the experiment.
4. Since the plasma renin concentration was normal, except during the short initial phase of stimulation, it is concluded that upon antibody injection the renin-angiotensin system rapidly, reached an equilibrium, with concentrations of free angiotensin close to or identical with normal concentrations.
Variation in the Proportions of Individual Pepsins Secreted by the Cat in Response to Vagal Stimulation and Hypoglycaemia
Authors: Wright Christine L. , Shaw B. , Sanders D. J. , Reed J. D. 
Published: August 2015

1. Gastric juice was collected at regular intervals during electrical stimulation of the vagus in anaesthetized cats and during insulin hypoglycaemia in both anaesthetized and conscious cats. The total amounts of acid and pepsin secreted were similar in the three groups.
2. Pepsins were examined by agar-gel electrophoresis. Resting juice contained two pepsins, and up to nine pepsins could be detected after stimulation. Three patterns of pepsin secretion were found.
3. The most noticeable feature was the variation in the proportion of total pepsin attributable to the pepsin which migrated most rapidly during electrophoresis (pepsin 1). In response to insulin hypoglycaemia, anaesthetized cats secreted only a small proportion of total pepsin as pepsin 1 and conscious cats secreted a large proportion as pepsin 1. During direct electrical stimulation of the vagus, the proportion of pepsin 1 rose.
4. The possibility of a dependence of pepsin 1 secretion on vagal stimulation is discussed and the relevance of this to peptic ulcer and to vagotomy is considered.
Blockade of Renin Release by Lanthanum
Authors: Logan A. G. , Tenyi I. , Quesada T. , Peart W. S. , Breathnach A. S. , Martin B. G. H. 
Published: August 2015

1. The effects of lanthanum on renin release and renal vasoconstriction were studied in the isolated perfused rat kidney.
2. Lanthanum reduced noradrenaline-induced renal vasoconstriction.
3. Lanthanum prevented isoprenaline-induced and glucagon-induced stimulation of renin secretion.
The Effect of Age on Deoxyribonucleic Acid Synthesis in Rat Adipose Tissue
Authors: Lewis B. M. , Hayes T. M. 
Published: August 2015

1. Rats of four different age groups were injected intraperitoneally with labelled thymidine and killed 1, 7 or 12 days later.
2. The epididymal fat-pads were separated into fat-cells and stromal elements by collagenase digestion.
3. The incorporation of labelled thymidine into the deoxyribonucleic acid (DNA) of both fractions was greatest in the 6-week-old animals. Uptake was significantly decreased in 12- and 15-week-old animals and was lowest in 22-week-old rats.
Oestrogen Hypertension in Rats
Authors: Saruta T. , Nakamura R. , Saito I. , Kondo K. , Matuki S. 
Published: August 2015

1. A large dose of oestrogen elevated the blood pressure in male Wistar rats.
2. Plasma renin substrate and renin activity increased significantly but plasma renin concentration was unchanged.
3. The increase in blood pressure induced by oestrogen was significantly reduced by salt loading, plasma renin concentration was suppressed and the increase in plasma renin activity was reduced.
4. The increase in plasma renin activity induced by the increase of plasma renin substrate concentration may play a role in oestrogen-induced elevation of blood pressure.
Effect of Parathyroid Extract on Renin Release in the Dog
Authors: McCredie D. A. , Powell H. R. , Rotenberg E. 
Published: August 2015

1. A rapid increase in plasma renin activity occurred in dogs after intravenous administration of parathyroid extract.
2. This was not seen after injection of a purer parathormone preparation, or the solution used to dilute the parathyroid extract or calcitonin.
3. A vasoactive compound in parathyroid extract appears to provide the most likely explanation of this effect.
Treatment of Patients with Severe Hypertension by Inhibition of Angiotensin-Converting Enzyme
Authors: Johnson J. G. , Black W. D. , Vukovich R. A. , Hatch F. E. , Friedman B. I. , Blackwell C. F. , Shenouda A. N. , Share L. , Shade R. E. , Acchiardo S. R. , Muirhead E. E. 
Published: August 2015

1. The results of the administration of the nonapeptide inhibitor (SQ 20,881) of the enzymatic conversion of angiotensin I into angiotensin II in twelve severe hypertensive patients are presented.
2. Administration of the compound was associated with a fall in blood pressure in ten of twelve patients.
3. Four patients had a normal plasma renin activity (PRA) with a range of 1.6–3.7 ng h−1 ml−1 and eight patients had a high PRA with a range of 5.0–74 ng h−1 ml−1. Two of the patients with normal PRA had no fall in blood pressure despite receiving 2 mg/kg of the compound. Two patients with normal PRA, however, did respond, thus indicating that a high PRA is not necessary for a response to the inhibitor compound.
4. It was found that haemodialysis or diuresis with frusemide enhanced the blood pressure response to the compound.
5. The presence of a measured low total blood volume was found to be associated with an exaggerated fall in blood pressure to a small dose of compound (0.125 mg/kg) in one patient.
The Use of Angiotensin-Converting Enzyme Inhibitor in the Diagnosis and Treatment of Hypertension
Authors: Gavras H. , Brunner H. R. , Laragh J. H. , Gavras I. , Vukovich R. A. 
Published: August 2015

1. The anti-hypertensive effect of converting enzyme inhibition was evaluated in twenty-three hypertensive patients (seven renovascular, four essential, four malignant, one scleroderma, three chronic renal failure, four primary or idiopathic aldosteronism).
2. In sixteen patients a single injection (1–4 mg/kg) of the inhibitor produced an immediate anti-hypertensive effect, which lasted up to 16 h. In six patients the anti-hypertensive effect of the inhibitor was significantly improved after sodium depletion.
3. Plasma renin activities increased and plasma aldosterone concentrations decreased consistently except in idiopathic aldosteronism.
4. Converting enzyme inhibition provides a direct way of defining the degree of renin-dependency of the hypertension. Accordingly, it can be used diagnostically and for planning appropriate therapy. Therapeutically, it could be advantageous in hypertensive emergencies because of its safety, specificity and capacity to reduce aldosterone secretion.
Long-Term Propranolol Treatment of Resistant Arterial Hypertension in Haemodialysed Patients
Authors: Maggiore Q. , Biagini M. , Zoccali C. , Misefari M. 
Published: August 2015

1. Propranolol was given to eight haemodialysed patients with resistant arterial hypertension for periods ranging from 6 to 16 months.
2. The treatment brought about an excellent control of blood pressure in all cases.
3. After withdrawal of propranolol plasma renin activity rose on average 40% compared with the value obtained during treatment. However, no significant relationship was found between the change in plasma renin activity and the change in the diastolic blood pressure.
4. Stopping propranolol resulted in a prompt rebound of arterial pressure toward pretreatment values. However, hypertension was always controlled on resuming drug treatment.
5. The results show that this form of hypertension can be controlled on a long-term basis with propranolol. However, the effect on blood pressure seems not to be mediated by suppression of renin secretion.
Effect of Oxprenolol on Catecholamines and Plasma Renin Activity: Acute Response to Frusemide in Hypertensive Patients
Authors: Muiesan G. , Alicandri C. , Rosei E. Agabiti , Motolese M. , Valori C. 
Published: August 2015

1. Catecholamine plasma concentrations and urinary excretion were measured together with plasma renin activity in ten patients with essential hypertension and in five normal control subjects before and after a frusemide challenge.
2. The same procedure was repeated in the same subjects 3–4 days later after pretreatment with oxprenolol.
3. Noradrenaline plasma concentrations and urinary excretion increased significantly after frusemide in all cases, returning to normal values at 30 and 60 min. Adrenaline plasma concentrations and urinary excretion were unchanged.
4. Plasma renin activity increased significantly in seven patients with hypertension and normal renin basal values, remaining unchanged in three hypertensive patients with low-renin basal values.
5. Oxprenolol suppressed the response of noradrenaline and plasma renin activity to frusemide in all cases.
Beta-Adrenergic Receptors and Renin Release: Studies with Beta-Adrenoreceptor-Blocking Agents in the Conscious Rabbit
Authors: Weber M. A. , Oates Helen F. , Stokes G. S. 
Published: August 2015

1. Plasma renin activity (PRA) and mean blood pressure were studied in conscious rabbits infused with beta-adrenoreceptor antagonists.
2. Oxprenolol and dl-propranolol each significantly reduced PRA and blood pressure, but prindolol, which had a strong blood pressure-lowering effect, increased PRA.
3. When prindolol was given to animals in which PRA and blood pressure had been reduced by dl-propranolol, PRA returned to control values but blood pressure remained low. Thus the increase in PRA caused by prindolol is not mediated by hypotension. These findings, together with the observation that compound H35/25 reduced PRA without altering blood pressure, suggest that the effects of the beta-adrenoreceptor-blocking drugs on blood pressure are unrelated to their effects on renin release.
4. Studies with d-propranolol and with blocking agents with either beta-1 or beta-2 specificity indicated that the effects of beta-adrenoreceptor blockade on renin are directly dependent upon their action on beta-adrenergic receptors, probably of the beta-2 type.
Effect of Propranolol on Blood Pressure in Normal and Hypertensive Rats
Authors: Conway J. , Darwin K. , Hilditch A. , Loveday B. , Reeves M. 
Published: August 2015

1. Propranolol has been given orally in a dose sufficient to achieve beta-blockade throughout the day in normal rats, renal hypertensive animals with and without contralateral nephrectomy, spontaneously hypertensive and deoxycorticosterone (DOCA) hypertensive rats. The drug was given either after hypertension had become fully established or during the phase of rising blood pressure.
2. With this treatment, heart rate was reduced by approximately 100 beats/min in all experimental groups.
3. In established hypertension, treatment with propranolol for 7–9 days was ineffective in lowering blood pressure in any of the models of experimental hypertension. It also had no effect on blood pressure in normal animals.
4. Chronic treatment with propranolol during the phase of rising blood pressure had no effect in renal hypertensive animals. In spontaneous hypertension, the rise in blood pressure was limited to 28 mmHg with propranolol treatment as compared with 58 mmHg in control animals. Likewise, in DOCA hypertension, the rise in pressure was limited to 18 mmHg as compared with 46 mmHg in control animals.
Plasma Renin, Urinary Sodium Excretion and Vascular Disease
Authors: Doyle A. E. , Chua K. G. , Duffy S. , Louis W. J. 
Published: August 2015

1. Urinary sodium excretion and plasma renin activity have been measured in a group of persons with untreated mild hypertension and in a control normotensive group.
2. Preliminary analyses of the data indicate that the daily sodium excretion was significantly higher in the hypertensive group but the plasma renin activity did not correlate significantly with the urinary excretion of sodium.
3. These findings suggest that sodium intake was significantly greater in a population with mild hypertension than in a comparable normotensive group.
Adrenergic Mechanisms in Human Hypertension and in Spontaneously Hypertensive Rats
Authors: Frohlich E. D. , Pfeffer M. A. 
Published: August 2015

1. The role of adrenergic neuronal mechanisms in the development of early hypertension in man and the spontaneously hypertensive rat has been explored.
2. In both, a hyperkinetic circulatory state is associated with reduced parasympathetic and increased adrenergic cardiac influences.
3. Spontaneously hypertensive and normotensive control rats were treated with propranolol from conception until 12 weeks. Although heart rate and output remained reduced, there was no difference in growth or elaboration of pressure with respect to their untreated controls.
4. After another series of spontaneously hypertensive and control rats received cardiac autonomic blockade (atropine and timolol), they sequentially received alpha-adrenergic blockade (phenoxybenzamine), ganglionic blockade (trimethaphan) and smooth-muscle vasodilatation (hydralazine). These studies revealed only a small pressure differential between the two groups before hydralazine and still less thereafter; unlike the control rats, pressure in spontaneously hypertensive rats fell markedly after ganglionic blockade as a result of reduced output, indicating greater adrenergic control mediated through venoconstriction.
5. These findings indicate: increased cardiovascular adrenergic control in young spontaneously hypertensive rats, the hyperkinetic circulation merely reflecting one aspect of increased total cardiovascular input. Structural alterations seem to participate minimally.
6. These experimental observations closely resemble findings in early hypertensive man, and it is suggested that altered total cardiovascular adrenergic input is responsible for the elaboration, development, and maintenance of essential hypertension in man.
Central Serotonergic Neurons and Experimental Neurogenic and Renal Hypertension in the Rabbit
Authors: Chalmers J. P. , Wing L. M. H. 
Published: August 2015

1. Rabbits received intracisternal injections of 5,6-dihydroxytryptamine (5,6-DHT) in order to ablate central serotonergic nerves and deplete central serotonin stores. Depletion was most marked in the spinal cord where serotonin concentration was reduced to less than 50% of that in rabbits given control injections.
2. In normal rabbits, intracisternal 5,6-DHT caused a transient reduction in arterial pressure, which was maximal 1 week after injection.
3. Intracisternal 5,6-DHT completely prevented the neurogenic hypertension produced by sinoaortic denervation in control animals and reversed it when given after sustained neurogenic hypertension had developed in denervated animals. These studies suggest that central serotonergic neurons participate in the baroreceptor reflex arc.
4. Intracisternal 5,6-DHT did not modify the renal hypertension that follows bilateral renal wrapping.
Renal Prostaglandin Synthesis in Experimental Renal-Clip Hypertension in the Rat
Authors: Pugsley D. , Beilin L. J. , Peto R. 
Published: August 2015

1. The hypothesis that suppression of prostaglandin E synthesis by indomethacin exacerbates renal-clip hypertension in the rat was investigated in four groups of rats.
2. Indomethacin was shown to exacerbate hypertension in renal-clip animals.
3. Synthesis of prostaglandin E, determined by gas-liquid chromatography, was suppressed in medullary tissue from the hypertensive animals irrespective of indomethacin treatment.
4. The findings support the concept that prostaglandins participate in the blood pressure regulatory function of the kidney but pose a number of unsolved questions.
Relation of Intracellular K+ and Steroidogenesis in Isolated Adrenal Zona Glomerulosa and Fasciculata Cells
Authors: Mendelsohn F. A. , Mackie C. 
Published: August 2015

1. Intracellular K+ content, water spaces and corticosterone output were measured in isolated zona glomerulosa and zona fasciculata-reticularis cell suspensions of rat adrenal cortex, after incubations in vitro under conditions designed to alter steroidogenesis.
2. Intracellular K+ of unpurified zona glomerulosa cells was not altered after stimulation of corticosterone output with serotonin. Similarly, with zona glomerulosa cells purified by unit gravity sedimentation, no change in intracellular K+ was detected after stimulation of steroidogenesis with serotonin or angiotensin II.
3. In high-potassium medium (final concentration 84 mmol/l), parallel increases in intracellular K+ and corticosterone output were observed with both unpurified and purified zona glomerulosa cells. However, a similar increase in intracellular K+ also occurred in high-potassium medium with zona fasciculata cells, whose steroid output is unresponsive to external potassium concentration ([K+]).
4. Ouabain at 10−5 mol/l depressed the intracellular [K+] of glomerulosa cells but did not alter basal or stimulated corticosterone output. Similar results were obtained with fasciculata cells.
5. Ouabain at 5×10−4 mol/l further depressed intracellular [K+] of glomerulosa cells and inhibited basal and stimulated corticosterone output. However, this concentration of ouabain also inhibited steroidogenesis in fasciculata cells.
6. These results demonstrate a variety of situations where changes in intracellular [K+] are dissociated from those in corticosterone output and indicate that intracellular [K+] cannot be the sole mechanism regulating steroidogenesis under these conditions.