bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ammonia and Urea Transport by the Excluded Human Colon
Authors: Bown R. L. , Gibson J. A. , Fenton J. C. B. , Snedden W. , Clark M. L. , Sladen G. E. 
Published: August 2015

1. Ammonia and urea transport across the colonic mucosa was studied by a perfusion technique in four subjects with colonic exclusion for chronic hepatic encephalopathy.
2. Reduction of luminal pH inhibited net and unidirectional transport of ammonia from lumen to plasma, but net absorption from high luminal concentrations persisted at low pH.
3. Neither addition of urea to the perfusate nor intravenous infusion of urea produced a consistent increase in the colonic excretion of ammonia when ammonia-free solutions were perfused.
4. In one subject intravenous infusion of [15N]-ammonium chloride produced rapid labelling of colonic effluent ammonia and within 60 min the specific enrichments of ammonia in effluent and in arterial plasma were approximately equal.
5. During perfusion of nitrogen-free solutions, only small amounts of urea appeared in the effluent, suggesting limited permeability of the colonic mucosa to urea.
6. These results are discussed in relation to the equilibration of ammonia across the colonic mucosa by both ionic and non-ionic diffusion. The lack of evidence of ‘juxtamucosal’ (as opposed to luminal) ureolysis is in contrast to other observations on the intact colon. The possible reasons for and implications of this discrepancy are discussed.
The Selective Inhibition of Chenodeoxycholate Synthesis by Cholate Metabolites in Man
Authors: Pomare E. W. , Low-Beer T. S. 
Published: August 2015

1. Seven normal volunteers took 0.28–0.42 mmol (100–150 mg) of deoxycholate by mouth. This resulted in a reduced proportion of chenodeoxycholate in bile and an increased proportion of deoxycholate. Cholate was unchanged. 2. Cholate and chenodeoxycholate pools and rates of synthesis were determined in four of the subjects by simultaneously labelling each pool with relabelled bile acids. The chenodeoxycholate pool and rate of synthesis decreased after deoxycholate administration. Cholate synthesis and pool size did not change appreciably.
3. The proportion of deoxycholate in bile samples of sixty-two subjects with intact enterohepatic circulation was found to be inversely related to the proportion of chenodeoxycholate in bile, but not to the cholate.
4. It is suggested that inhibition of chenodeoxycholate synthesis by deoxycholate, the principal bacterial product of cholate, regulates the size of the chenodeoxycholate pool independently of the total amount of bile salt.
Angiotensin Blockade in Studies of the Feedback Control of Renin Release in Rats and Rabbits
Authors: Stokes G. S. , Oates Helen F. , Weber M. A. 
Published: August 2015

1. In rabbits actively immunized against angiotensin II (AII), the appearance of anti-AII antibodies was associated with a rise in plasma renin activity (PRA), which did not occur in mock-immunized controls.
2. In conscious rabbits, infusion of the angiotensin inhibitor, Sar1-Ala8-angiotensin II (P-113), at rates of 0.055, 0.22 or 1.1 nmol min−1 kg−1 into the renal artery, caused dose-related increases in arterial PRA and renal arteriovenous PRA difference. Renal blood flow fell with the high dose, but not with the low or medium doses. A fall in arterial pressure, asynchronous with peak renin secretion, accompanied the medium- and high-dose infusions.
3. Intravenous infusion of inhibitor P-113, 5.5 nmol min−1 kg−1, into anaesthetized rats produced highly significant increases in PRA and plasma renin concentration without reduction in arterial pressure. There were no changes in PRA or plasma renin concentration in saline-infused control rats.
4. These findings suggest that AII blockade interrupts a negative feedback loop controlling renin secretion.
Factors affecting the Metabolic Production of Methylguanidine
Authors: Gonella M. , Barsotti G. , Lupetti S. , Giovannetti S. 
Published: August 2015

1. Methylguanidine administered orally to normal volunteers was almost completely recovered in the urine, indicating that it is absorbed in the gastrointestinal tract and is not converted into other compounds. In normal persons at least, its urinary output therefore corresponds to its metabolic production rate plus the amount ingested.
2. In normal persons, diets based on foods not containing methylguanidine (e.g. vegetarian, protein-free and milk-egg diets) caused a fall in the urinary output of methylguanidine as compared with the output of the same subjects on a free diet. Conversely, higher amounts of methylguanidine were excreted on a diet rich in broth and in boiled beef, which contain large amounts of methylguanidine formed from the oxidation of creatinine, caused by boiling.
3. Oral administration of creatinine to normal volunteers induced an immediate and marked increase in urinary excretion of methylguanidine, and the ingestion of [methyl-14C]creatinine by uraemic patients was followed by the urinary excretion of labelled methylguanidine. These findings indicate that creatinine is partly converted into methylguanidine in both normal and uraemic subjects and accounts for the high metabolic production of methylguanidine in patients with renal failure, in whom the body pool of creatinine is high.
4. Creatinine, incubated at 38°C for 24 h in Krebs bicarbonate solution (pH 7.38) through which was bubbled oxygen with 15% carbon dioxide, was partially oxidized to methylguanidine. This raises the possibility that even in vivo such a conversion may occur ‘non-enzymatically’.
Protein Synthetic Activity of Membrane-Bound and Free Ribosomes from Parathyroid Glands of Dogs
Authors: Alford F. P. , Cook P. S. , Swenson R. S. , Reaven G. M. 
Published: August 2015

1. Membrane-bound and free polyribosomes were isolated from parathyroid glands of normal dogs by a discontinuous density-gradient technique.
2. The conditions necessary for optimum incorporation by bound and free ribosomes of [3H]-phenylalanine into protein were determined for asays in vitro directed by both endogenous messenger ribonucleic acid (mRNA) and polyuridylic acid [poly(U)].
3. When the specific cofactors were available in optimum amounts, the rate of incorporation of amino acids into protein was directly proportional to the number of ribosomes present. This applied to assays directed by endogenous mRNA and poly-(U).
4. The results indicate that it is possible to isolate and directly study the protein synthetic activity of membrane-bound and free parathyroid ribosomes.
The Relationship of Body Fat Content to Deep Muscle Temperature and Isometric Endurance in Man
Authors: Petrofsky J. S. , Lind A. R. 
Published: August 2015

1. The relationship between body fat content, isometric endurance and deep muscle temperature was assessed in eight male and female volunteers trained to static effort.
2. Muscle temperature, measured in the belly of the brachioradialis muscle, was found to be directly related to the subjects' body fat content.
3. Associated with a reduction in body fat content, there was a marked decrease in deep muscle temperature and an increase in isometric endurance of the hand-grip muscles; no change in strength was noted.
4. Conversely, an increase in body fat content resulted in an increase in deep muscle temperature and a decrease in isometric endurance.
5. When muscle temperature was stabilized before and after weight loss by immersing the forearm in water at 37°C, a reduction in body fat no longer influenced endurance.
6. It was concluded that the change in isometric endurance associated with either loss or gain of weight can be accounted for entirely by the changes in muscle temperature.
Effects of Inhaled Prostaglandins E1, E2 and F2α on the Airway Resistance of Healthy and Asthmatic Man
Authors: Smith A. P. , Cuthbert M. F. , Dunlop L. S. 
Published: August 2015

1. Changes in specific airway conductance after the inhalation of aerosols of prostaglandins (PG) E1, E2 and F2α were investigated in healthy and asthmatic subjects.
2. Inhalation of 155 nmol (55 μg) of PGE1 or 156 nmol (55 μg) of PGE2 resulted in consistent minor bronchodilatation in healthy subjects, but in asthmatic patients airway conductance increased significantly, along with subjective improvement. Isoprenaline (988 nmol; 550 μg) inhalation resulted in a similar increase in conductance to that obtained after these two prostaglandins, whereas a control aerosol had no effect. In contrast to the isoprenaline aerosol, both PGE1 and PGE2 were highly irritant to inhale. It was concluded that this made them unsuitable for therapeutic use.
3. Prostaglandin F2α inhalation resulted in a dose-related bronchoconstriction in healthy and asthmatic subjects. Asthmatics were approximately 150 times more sensitive to PGF2α than were the healthy subjects but there was very wide and significant variation in the sensitivity of the asthmatic subjects. In contrast the asthmatic subjects were only 8.5 times more sensitive to histamine than the healthy subjects with less variation in response of individual subjects. The reasons for the hyper-reactivity of asthmatic subjects to PGF2α is unknown and no correlation could be drawn between increased sensitivity and age, type of asthma, or treatment.
4. The effects of disodium cromoglycate, flufenamic acid, atropine methonitrate, PGE2 and isoprenaline on PGF2α-induced bronchoconstriction were investigated in healthy subjects. Prostaglandin E2 reversed PGF2α-induced bronchoconstriction, as did isoprenaline, but prior treatment with the other drugs had no effect in preventing bronchoconstriction.
Hypertensive and Renin-Suppressing Activities of Propranolol in Hypertensive Patients
Authors: Leonetti G. , Mayer Genevieve , Morganti A. , Terzoli Laura , Zanchetti A. , Bianchetti G. , Di Salle E. , Morselli P. L. , Chidsey C. A. 
Published: August 2015

1. In patients with mild or moderate essential hypertension, oral propranolol, given in incremental doses, produced a moderate but significant lowering of blood pressure which was correlated with the concentration of propranolol in plasma.
2. Propranolol also reduced plasma renin activity (PRA) in the supine posture, on standing and after intravenous frusemide. However, ‘supine’ and ‘frusemide’ PRA values were markedly reduced at a plasma concentration of propranolol that had little effect on blood pressure.
3. On administration of propranolol there was little correlation between blood pressure decrease and PRA suppression, and even less between pretreatment PRA values and hypotensive response.
4. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, suppression of PRA is not an important determinant of the hypotensive response to propranolol.
The Role of the Renin—Angiotensin—Aldosterone System in Cardiovascular Homeostasis in Normal Man
Authors: Haber E. , Sancho J. , Re R. , Burton J. , Barger A. C. 
Published: August 2015

1. To examine the role of angiotensin II in the maintenance of blood pressure and control of aldosterone secretion, eight normal human subjects were studied on a tilt table in sodium-replete and sodium-depleted states, before and after the administration of an angiotensin converting-enzyme inhibitor (CEI).
2. Administration of CEI was followed by a marked fall in blood pressure on tilting in sodium-depleted, but not in sodium-replete, subjects. CEI administration also resulted in a rise in plasma renin activity in the supine position, in the absence of haemodynamic change. The rise in plasma aldosterone observed both in response to tilting and sodium depletion did not occur after CEI, even though plasma renin activities were higher.
3. These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture.
Renin-Suppressive Potency of Various Beta-Adrenergic Blocking Agents at Supine Rest and during Upright Exercise
Authors: Bühler F. R. , Marbet G. , Patel U. , Burkart F. 
Published: August 2015

1. Renin responses to different types of beta-adrenergic blocking agents were compared in eight normal volunteers at supine rest and during moderate upright exercise.
2. Comparable beta-adrenergic blockade was achieved with equipotent cardiodeceleratory doses of 100 mg of propranolol, 400 mg of practolol, 100 mg of oxprenolol, 10 mg of timolol, 5 mg of pindolol or 100 mg of ICI 66082.
3. All beta-blocking agents tested significantly and markedly reduced plasma renin activity during upright exercise. Renin suppression was not related to either β1- or β2-type receptor blocking action.
4. Renin levels at rest were generally reduced by the blocking drugs, but these responses did not reach significance for oxprenolol and pindolol. With both these drugs, lesser suppressibility of basal renin may be due to their inherent sympathomimetic activity.
5. The results suggest that different types of beta-blocking agents suppress plasma renin activity and therefore that they all may lower blood pressure through reduction of angiotensin vasoconstriction.
Effect of Volume Depletion and Subsequent Propranolol Treatment on Blood Pressure and Plasma Renin Activity in Patients with Essential and with Renovascular Hypertension
Authors: Geyskes G. G. , Boer P. , Leenen F. H. H. , Mees E. J. Dorhout 
Published: August 2015

1. In nineteen patients, five with unilateral renal artery stenosis and fourteen with essential hypertension (WHO grades I–II), blood pressure, plasma and extracellular fluid volumes and plasma renin activity were studied at the end of three sequential periods: (a) after at least 3 days on a 60 mmol Na+ diet; (b) after 3 days of salt depletion induced with a diuretic and sustained on a 20 mmol Na+ diet; (c) after 3 days during which the 20 mmol Na+ diet was continued and beta-receptor blockade was induced by increasing dosages of propranolol up to 320 mg daily.
2. After sodium depletion extracellular fluid volume and plasma volume decreased and plasma renin activity increased; blood pressure did not change significantly.
3. After adding propranolol, plasma volume and extracellular fluid volume remained low, and there was a significant decrease in plasma renin activity and blood pressure.
4. No correlation could be demonstrated between changes of blood pressure and plasma renin activity.
5. When the responses of the five patients with renal artery stenosis were compared with those of the fourteen patients with essential hypertension, no significant differences were found.
6. Propranolol has a strong anti-hypertensive effect after Na+ depletion, irrespective of the absolute activities of plasma renin.
Blood Pressure Decrease and Responsiveness to Renin-Releasing Stimuli under Increasing Doses of Propranolol in Patients with Essential Hypertension
Authors: Leonetti G. , Mayer G. , Morganti A. , Terzoli L. , Zanchetti A. , Morselli P. L. , Di Salle E. , Chidsey C. A. 
Published: August 2015

1. Stepwise increases of oral doses of propranolol produced both a significant lowering of blood pressure and suppression of plasma renin activity in sixteen patients with mild or moderate normal-renin essential hypertension.
2. The hypotensive and the renin-suppressive actions of propranolol were differently related to plasma propranolol concentrations. At the lowest propranolol concentrations (15–40 nmol/l), there was almost no decrease in blood pressure whereas plasma renin activity and responsiveness to renin-releasing stimuli (standing, intravenous frusemide) were already strongly depressed (greater than 50%). Therefore in a large number of normal-renin hypertensive patients under small doses of propranolol, the renin-suppressive action of the drug can be dissociated from the hypotensive effect. Dissociation of the two effects, though in the opposite way, was also observed in three of four low-renin hypertensive patients, whose blood pressure was decreased by propranolol without further reduction of the already suppressed plasma renin activity.
3. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, the hypotensive effect of propranolol cannot be attributed to suppression of renin activity. These conclusions do not necessarily apply to high-renin hypertensive patients.
Beta-Blocking Drugs and Renin Secretion in the Anaesthetized Dog
Authors: Imbs J. L. , Kraetz J. , Schmidt M. , Desaulles E. , Schwartz J. 
Published: August 2015

1. The effect of propranolol and sotalol on renin secretion was studied in the anaesthetized dog.
2. Beta-adrenergic blockade did not modify basal renin secretion and did not affect the rise of renin secretion induced by haemorrhage or aortic constriction.
3. Beta-adrenergic blockade diminished the rise in renin secretion induced by stimulation of the renal nerves.
Pathogenesis and Prevention of Stroke in Spontaneously Hypertensive Rats
Authors: Okamoto K. , Hazama F. , Yamori Y. , Haebara H. , Nagaoka A. 
Published: August 2015

1. A colony of stroke-prone spontaneously hypertensive rats has been developed by selective breeding.
2. These animals developed severe hypertension early in life, the magnitude of the hypertension being closely related to the incidence of stroke.
3. No evidence was obtained of any humoral factor responsible for strokes.
4. Local factors predisposing to stroke were a scanty arterial supply with characteristic recurrent branching of long and large arteries, together with increased vascular permeability, angio-necrosis, and formation of microaneurysms.
5. Strokes could be prevented by adequate anti-hypertensive therapy from an early age.
Effect of Pyratrione (a Tyrosine Hydroxylase Inhibitor) in Essential Hypertension
Authors: Kimura T. , Takahashi E. , Ozawa M. , Uchiyama S. , Maekawa S. , Yashima O. , Sato M. 
Published: August 2015

1. A clinical study of pyratrione, a tyrosine hydroxylase inhibitor, has been carried out in essential hypertension.
2. Out of thirty-nine patients who received pyratrione, twenty-eight showed a significant decrease in blood pressure.
The Use of Minoxidil, an Experimental Arteriolar Dilator, in 510 Patients with Refractory Hypertension
Authors: Martin W. B. , Zins G. R. , Freyburger W. A. 
Published: August 2015

1. Minoxidil, an experimental arteriolar dilator, has been used in conjunction with a diuretic and a sympathetic nervous system suppressant in 510 patients with refractory hypertension, of whom 323 remain on treatment. The results in two of a total of twenty aetiological groups are described.
2. Of eighty-eight patients with refractory hypertension who were on maintenance haemodialysis when minoxidil was first administered, forty-six currently remain on treatment. In these the average blood pressure fell to 150/100 mmHg from an average of 190/130 mmHg before minoxidil. Healing occurred in the nineteen who had had grade 3 or 4 optic fundi. Side effects resulted in discontinuation of the drug in four of the eighty-eight patients.
3. Thirty-five patients with essential hypertension and good renal function were treated for from 3 to 12 months. The supine blood pressures before minoxidil averaged 280/128 mmHg and averaged 160/97 mmHg whilst the drug was given. The serum creatinine concentration did not change significantly. The optic fundi improved in nine; in nine others episodes of congestive heart failure were reduced in frequency.
4. If careful attention is directed to salt balance and to heart rate, minoxidil may help control otherwise refractory hypertension.
Central Regulation of Arterial Blood Pressure
Authors: Philippu A. 
Published: August 2015

1. Cats were anaesthetized with pentobarbitone sodium. The hypothalamus was superfused with drugs through a push-pull cannula and electrically stimulated with the non-insulated tip of the cannula. In another series of experiments, the hypothalamus was stimulated with a monopolar electrode and the nucleus of the solitary tract superfused with drugs through a push-pull cannula.
2. Superfusion of the hypothalamus with alpha-adrenoreceptor blocking agents (piperoxan or tolazoline) decreased the pressor responses to hypothalamic stimulation. Superfusion with low concentrations of clonidine increased, whereas superfusion with higher concentrations of this drug diminished, the rise of blood pressure during hypothalamic stimulation. Muscarinic agents (oxotremorine, muscarine or AHR 602) decreased the pressor responses to hypothalamic stimulation. The inhibitory effects of the muscarinic compounds were abolished by superfusing the hypothalamus with methylatropine. Superfusion with nicotinic agents (1,1-dimethyl-4-phenylpiperazinium, or carbachol) enhanced the pressor responses to hypothalamic stimulation. The enhancement of the pressor responses by these drugs was completely inhibited by superfusion of the hypothalamus with hexamethonium.
3. Superfusion of the nucleus of the solitary tract with tolazoline enhanced the pressor responses to hypothalamic stimulation. The pressor responses were reduced during superfusion of the nucleus of the solitary tract with clonidine.
Neural Control of Renin Release
Authors: Zanchetti A. , Stella A. 
Published: August 2015

1. Factors involved in the neural control of renin release have been reviewed.
2. Experimental evidence has been obtained that sympathetic stimulation releases renin from the kidney independently of local vasomotor changes.
3. The reflex control of renin release on postural change has been established.
4. The effect of diuretics on renin release has been studied and evidence of neural and non-neural mechanisms obtained.
5. The effect of suprarenal aortic stenosis has been studied; the findings suggest that renin release is in some way dependent on neural mechanisms.
6. The pathological significance of the neural control of renin release has been discussed.
Plasma Noradrenaline Concentration and Blood Pressure in Essential Hypertension, Phaeochromocytoma and Depression
Authors: Louis W. J. , Doyle A. E. , Anavekar S. N. 
Published: August 2015

1. Mean plasma noradrenaline concentration was elevated in forty-four patients with established essential hypertension. Eighteen of these hypertensive patients had resting plasma noradrenaline concentrations in the normal range.
2. Patients with endogenous depression had higher mean plasma noradrenaline concentrations but significantly lower blood pressure than patients with essential hypertension.
3. Patients with phaeochromocytoma had plasma noradrenaline concentrations twenty-eight times greater than those found in essential hypertension, but blood pressures were less than 20% higher.
4. It is concluded that excess of sympathetic drive only partly explains the level of the blood pressure in essential hypertension.
Role of the Autonomic Nervous System in Mild Human Hypertension
Authors: Julius S. , Esler M. D. , Randall O. S. 
Published: August 2015

1. Some of the haemodynamic abnormalities in mild (borderline) human hypertension appear to be neurogenic, since they can be completely abolished by pharmacological autonomic blockade.
2. The cardiac output is elevated in 30% of patients through increased sympathetic drive and decreased parasympathetic inhibition.
3. In the remainder, the higher blood pressure is maintained by increased total peripheral vascular resistance.
4. In approximately 30% of this latter group, the higher vascular resistance is maintained solely by increased alpha-adrenergic tone.
5. Elevated plasma renin activities in a proportion of cases are probably due to generalized increase in sympathetic nervous activity.
6. Patients with mild hypertension thus show increased sympathetic drive to the heart and arterioles as well as decreased cardiac parasympathetic inhibition. It is presumed that the increased plasma renin is also neurogenic.
7. Such a widespread distribution of altered autonomic tone suggests aberration of the function of the integrative centres of cardiovascular control.
8. Evidence is presented of a possible psychosomatic origin of these changes in some cases.