bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ambulant Blood Pressure: Reproducibility and the Assessment of Interventions
Authors: Mann S. , Craig M. W. Millar , Balasubramanian V. , Cashman P. M. M. , Raftery E. B. 
Published: August 2015

1. We have assessed the day-to-day reproducibility of intra-arterial blood pressure by monitoring 17 freely ambulant hypertensive patients for a period of 48 h. Eight had no change of therapeutic regimen throughout and nine took a single dose of a hypotensive agent before retiring on the second night.
2. Records were analysed to provide hourly mean values of heart rate, systolic and diastolic blood pressure. No significant differences between first and second day recordings were found except after the intervention in the second group.
3. Allowing subjects to follow their normal daily routine produces inevitable variation in their pattern of physical and other activity. However, by the use of these methods of recording and analysis, with pooled measurements from a small group of subjects, reproducibility is sufficiently good to permit the reliable assessment of therapeutic interventions.
The Effect of the Methionine Enkephalin Analogue DAMME on the Vasopressin Response to Tilt in Man
Authors: Lightman S. L. , Forsling Mary L. 
Published: August 2015

1. Infusion of the methionine enkephalin analogue DAMME (Sandoz) inhibits the rise in plasma arginine vasopressin after a 65° head-up tilt.
2. DAMME does not significantly affect the blood pressure, pulse rate or plasma volume changes produced by tilt.
Brain Angiotensin II Stimulates Release of Pituitary Hormones, Plasma Catecholamines and Increases Blood Pressure in Dogs
Authors: Schölkens B. A. , Jung W. , Rascher W. , Schömig A. , Ganten D. 
Published: August 2015

1. The mechanisms of central angiotensin II blood pressure effects in conscious dogs on normal or sodium-deficient diets were examined.
2. The biosynthesis of brain angiotensin II in cerebrospinal fluid from its local precursor angiotensinogen was induced in vivo by injection of 0.5 unit of hog kidney renin through a chronically implanted cannula into the third brain ventricle in conscious dogs.
3. Intracerebroventricular administration of renin induced an increase of arterial blood pressure and a marked drinking response under both dietary regimens. Sodium restriction had no effect on the magnitude of the central angiotensin pressor response.
4. Plasma concentrations of renin and angiotensin II decreased, and plasma antidiuretic hormone, noradrenaline, adrenaline and corticosterone increased, in both groups of dogs.
5. Simultaneous intraventricular administrations of captopril with renin inhibited the central renin effects. Intracerebroventricular injections of [Sar1, Val5, Ala8] angiotensin II alone increased plasma renin and angiotensin II concentrations.
6. It is concluded that endogenous brain angiotensin II participates in central mechanisms of blood pressure regulation by the stimulation of the release of antidiuretic hormone, adrenocorticotrophic hormone, adrenaline and noradrenaline.
Angiotensin II in Human Cerebrospinal Fluid May Be An Immunoassay Artifact
Authors: Semple P. F. , MacRae W. A. , Morton J. J. 
Published: August 2015

1. Concentrations of angiotensin II (ANG II) were measured by radioimmunoassay in cerebrospinal fluid and plasma from neurosurgical patients and patients having spinal anaesthesia. Cerebrospinal fluid concentrations of renin, renin substrate and ANG I were also measured.
2. Cerebrospinal fluid concentrations of ANG II measured with antiserum 30/VI were low in neurosurgical patients (mean 6 pmol/l, range &lt; 2-12 pmol/l, n = 7) and lower in spinal anaesthesia patients (mean 1 pmol/l, range &lt; 2–4 pmol/l, n = 14) and unrelated to concurrent plasma concentrations of ANG II.
3. A second more sensitive immunoassay with ANG II antiserum 9/P gave higher cerebrospinal fluid concentrations of ANG II in spinal anaesthesia patients (mean 15 ± 1 pmol/l, n = 7, P &lt; 0.01).
4. Paper chromatography showed that the ANG II immunoreactive material measured with antiserum 9/P was not ANG I, ANG II, ANG II-(2-8), ANG II-(3-8) or ANG II-(4-8).
5. The concentration of ANG I in cerebrospinal fluid was low (4 ± 0.04 pmol/l, n = 7). No renin was detected (n = 32) and the concentration of renin substrate was 45 ± 2.6 nmol/l (n = 24).
6. Much of the immunoreactive ANG II in human cerebrospinal fluid is an immunoassay artifact
Adrenal Angiotensin II Receptors and Vascular Reactivity to Angiotensin II in the Rat during Continuous Inhibition of Angiotensin Converting Enzyme
Authors: Millar J. A. , Casey D. J. , Johnston C. I. 
Published: August 2015

1. The effect of continuous infusion of captopril (80 μg/h) for up to 5 days on blood pressure, adrenal angiotensin II receptors and vascular reactivity to exogenous angiotensin II, arginine vasopressin and noradrenaline was studied in the rat.
2. In treated rats, blood pressure decreased transiently to a minimum after 2 days (−18 mmHg). Vascular reactivity to angiotensin II, but not to arginine vasopressin, was also increased significantly after 2 days, but vascular reactivity to noradrenaline decreased. After 5 days, vascular reactivity to angiotensin II had returned to normal and was similar to that of sham-treated controls. Adrenal angiotensin II receptor concentrations decreased significantly after 1 and 2 days, but at 5 days were again similar to controls. There was no change in receptor affinity.
3. Converting enzyme inhibition with captopril causes transient specific changes in adrenal angiotensin II receptors and vascular reactivity. The receptor and vascular effects may facilitate and oppose, respectively, the early changes in blood pressure with captopril, but a long-term contribution from either is unlikely.
Captopril Affects Blood Pressure Equally in Renovascular and Essential Hypertension and in the Fluid-Depleted Anephric State
Authors: De Bruyn J. H. B. , Wenting G. J. , Man in 'T Veld A. J. , Derkx F. H. M. , Schalekamp M. A. D. H. 
Published: August 2015

1. The haemodynamic effects of 100 mg of captopril in renovascular hypertension (n = 11), essential hypertension (n = 12) and the anephric state (n = 7) were compared. Brachial artery pressure was measured in all patients, and changes in right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure and cardiac output were followed in renovascular and essential hypertension. Nephrectomized patients were studied before and after fluid withdrawal by ultrafiltration.
2. The pretreatment concentration of active renin in plasma was 100 ± 24 μ-units/ml (mean ± sem) in renovascular hypertension, and 24 ± 4 μ-units/ml in essential hypertension. In nephrectomized patients pretreatment renin was 1.7 ± 0.3 μ-units/ml, and renin was unresponsive to withdrawal of 1.8 ± 0.2 1 of body fluid.
3. The effects of captopril were maximal after 60–90 min. Mean arterial pressure after 90 min was lowered by 19 ± 4% in renovascular hypertension, by 17 ± 4% in essential hypertension and by 16 ± 3% in fluid-depleted nephrectomized patients. These changes were not significantly different despite the marked differences in renin. Captopril had no effect on arterial pressure in the fluid-replete anephric state.
4. The effects of captopril on cardiac filling pressures and cardiac output in renovascular and essential hypertension were also not different.
5. It is concluded that the antihypertensive action of captopril may be largely independent of circulating renin.
Effects of β-Lipotropin on Aldosterone Production in Rats
Authors: Matsuoka Hiroaki , Mulrow Patrick J. , Franco-Saenz Roberto , Li Choh Hao 
Published: August 2015

1. β-Lipotropin has a potent aldosterone stimulating effect in vitro and in vivo in rats.
2. The maximum aldosterone response to β-lipotropin was the same as to ACTH and greater than to angiotensin II.
3. Although doses of ACTH which maximally stimulated aldosterone significantly increased cyclic AMP production, maximally stimulating doses of sheep β-lipotropin did not increase cyclic AMP production significantly.
4. These data suggest that β-lipotropin may play a role in aldosterone regulation through a mechanism different from that of ACTH.
Interactions of Prostaglandins with the Kallikrein-Kinin and Renin-Angiotensin Systems
Authors: McGiff J. C. 
Published: August 2015

1. Prostaglandins together with the kallikrein-kinin system comprise a major vasodepressor system.
2. Prostaglandins can antagonize the actions of pressor hormones and the adrenergic nervous system. They also contribute to the blood pressure-lowering effects of kinins by enhancing the vasodilator and diuretic-natriuretic actions of the peptide.
3. Deficiency of the vasodepressor system may lead to hypertension without any increase in the basal activity of the blood pressure-elevating system.
4. Increased activity of the renin-angiotensin and adrenergic nervous systems evoked by stressful stimuli enhances prostaglandin synthesis, which protects organ function from excessive effects of angiotensins and catecholamines.
5. Several findings preclude unqualified acceptance of prostacyclin as the only important vascular prostaglandin: first, in some blood vessels prostacyclin is not the principal product of enzymic transformation of the cyclic endoperoxides. Secondly, prostaglandin E2, which is also synthesized in the vascular wall, may be the principal modulator prostaglandin. Lastly, prostacyclin may be transformed by some tissues to 6-keto-prostaglandin E1, a more stable product having similar biological potency.
6. Synthesis of prostaglandins by the kidney is important to mechanisms which control renin release and renal vascular resistance.
Circulating Prostacyclin Concentrations May Be Increased by Bendrofluazide in Patients with Essential Hypertension
Authors: Webster J. , Dollery C. T. , Hensby C. N. 
Published: August 2015

1. A within-patient randomized double-blind crossover study was performed on mechanisms of action of bendrofluazide in mild essential hypertension. Significant reductions in lying, standing and post-exercise blood pressure were seen after both 3 days and 10 weeks treatment with bendrofluazide (10 mg daily).
2. Plasma levels of 6-oxo-prostaglandin F1α, the chemical hydrolysis product of prostacyclin, were significantly increased by both 3 days and 10 weeks therapy with bendrofluazide. This raises the possibility that thiazides may reduce peripheral resistance by increasing prostacyclin biosynthesis.
Inhibition by Bradykinin of the Vascular Effects of Pressor Hormones in the Canine Kidney: Relationship to Prostaglandins
Authors: Sušić H. , Nasjletti A. , Malik K. U. 
Published: August 2015

1. Renal arterial injection of bolus doses of angiotensin II or noradrenaline, (0.06, 0.12 and 0.25 μg) caused renal vasoconstriction and decreased blood flow to the kidney in a dose-related manner in dogs anaesthetized by sodium pentobarbital.
2. The effect of angiotensin II and noradrenaline in lowering renal blood flow was reduced during renal arterial infusion of either bradykinin (10 ng min−1 kg−1) or prostaglandin E2 (4 ng min−1 kg−1).
3. Pretreatment of the dogs with an inhibitor of prostaglandin synthesis, sodium meclofenamate (5 mg/kg), blunted the inhibitory action of bradykinin, but not that of prostaglandin E2, on renal vascular reactivity to angiotensin II and noradrenaline.
4. These results indicate that bradykinin reduces the renal vasoconstriction induced by angiotensin II and noradrenaline in the dog by a mechanism dependent upon synthesis of prostaglandins.
Blood Volume and Interstitial Fluid Pressure in the Development and Reversal of Renal Hypertension in Rats
Authors: Trippodo N. C. , Ziegler L. P. 
Published: August 2015

1. During the development and maintenance of one-kidney, one-clip hypertension in rats, there were no significant differences in blood volume or interstitial fluid pressure compared with one-kidney control rats.
2. Rats with one-kidney, one-clip hypertension of 25 days' duration were either unclipped, sham-operated or nephrectomized. Over 24 h the changes in arterial pressure, blood volume and interstitial pressure in the sham and nephrectomized groups were insignificant. In the unclipped group arterial pressure decreased 50 mmHg to normal by 24 h and was associated with increased diuresis and a small decrease in blood volume (9.8%). Unclipped rats with the greatest urine outputs showed the largest decreases in interstitial pressure (r = 0.70, P&lt;0.02).
3. Thus, in the reversal of this hypertension, changes in blood volume played only a partial role; decreased interstitial pressure was secondary to tissue fluid depletion from increased diuresis and normalization of arterial pressure required the presence of the unclipped kidney.
Effect of Inheritance and Stress on the Diurnal Excretion of Sodium and Potassium in Young People with and without a Family History of Hypertension
Authors: Parfrey P. S. , Wright P. , Ledingham J. M. 
Published: August 2015

1. The diurnal excretion of sodium and potassium was observed in young people, with and without a genetic predisposition to hypertension, both in the presence and absence of psychological stress.
2. In the absence of stress, the normal day/night sodium excretion ratio was reversed in the children of hypertensive parents. This was significantly less than day/night sodium excretion in children of normotensive parents. A similar finding was observed for day/night potassium excretion.
3. There was a significant negative correlation between systolic blood pressure and day/night sodium excretion in children of hypertensive parents but not in children of normotensive parents.
4. After the mental stress of a University examination day/night sodium reverted to normal in children of hypertensive parents.
Sodium—Potassium-Dependent ATPase Activity in Erythrocyte Ghosts of Patients with Primary and Secondary Hypertension
Authors: Wambach G. , Helber A. , Bounner G. , Hummerich W. , Konrads A. , Kaufmann W. 
Published: August 2015

1. We have investigated the function of the Na+-K+ pump in the erythrocytes of patients with various types of hypertension by measuring the activity of ouabain-sensitive Na+-K+-dependent ATPase and ouabain-insensitive ATPase in the erythrocyte ghosts of these patients.
2. Mean Na+-K+-ATPase activity was increased threefold in six patients with Cushing's syndrome and hypertension (0.985 ± sd 0.288 μmol of phosphate h−1 mg−1) compared with that in 49 control subjects (0.334 ± 0.147 μmol of phosphate h−1 mg−1) (P&lt;0.0025), but not in four patients with primary aldosteronism (0.278 ± 0.108 μmol of phosphate h−1 mg−1).
3. Na+-K+-ATPase activity slightly exceeded the control range in 57 patients with primary hypertension (0.410 ± 0.245 μmol of phosphate h−1 mg−1; P&lt;0.025) and in 12 patients with renal hypertension (0.475 ± 0.250 μmol of phosphate h−1 mg−1) (P&lt;0.025).
4. There was no difference in ouabain-insensitive ATPase between the controls and the different types of hypertension.
5. The data support the hypothesis of an activation of the Na+ pump in patients with glucocorticoid excess. This helps to explain previous observations of a redistribution of sodium and water to the extracellular compartment in experimental glucocorticoid-induced hypertension.
Studies on the Role of Sodium-Potassium-Activated ATPase as Determinant of Vascular Reactivity in Wistar-Kyoto and Spontaneously Hypertensive Rats
Authors: Gouthberg G. , Jandhyala B. , Folkow B. 
Published: August 2015

1. The role of Na+-K+-activated ATPase in the regulation of resistance vessel reactivity to barium chloride and noradrenaline was investigated with a pair-perfused hindquarter technique in spontaneously hypertensive rats and Wistar-Kyoto rats (6 and 12 week old). Ouabain (10−4 mol/l) was used to inhibit the sodium pump.
2. In all groups studied, dose-response curves to agonists were shifted to the left when ouabain was added to the perfusion medium. This potentiation in vascular reactivity produced by ouabain was expressed as ‘index for sodium-pump inhibition’ (ISPI = ED50 of an agonist/ED50 + ouabain).
3. In mature rats index for sodium-pump inhibition calculated for both agonists was significantly greater in spontaneously hypertensive rats in comparison with Wistar-Kyoto rats, but not so in young spontaneously hypertensive rats. There was, however, a trend towards increased noradrenaline sensitivity in spontaneously hypertensive rats although the difference from Wistar-Kyoto rats was not statistically significant.
4. The data may suggest that there is some increase in the activity of the sodium pump in the resistance vessels of mature spontaneously hypertensive rats, perhaps to compensate for an increased passive sodium permeability.
Erythrocyte 22Na Efflux and Urinary Sodium Excretion in Essential Hypertension
Authors: Fitzgibbon W. R. , Morgan T. O. , Myers J. B. 
Published: August 2015

1. The rate constant for total 22Na efflux from erythrocytes was examined in patients with mild to moderate hypertension and in normotensive controls. No difference in 22Na efflux rate constant was found when the cells from both groups were incubated in artificial medium. When the cells from both groups were incubated in their own plasma, the rate constant for Na efflux was significantly elevated for hypertensive patients compared with controls (0.40 ± 0.02, 0.36 ± 0.01 respectively; P&lt;0.05).
2. In hypertensive patients sodium efflux rate constant varied inversely with 24 h urinary sodium excretion when erythrocytes were incubated in artificial medium (r = − 0.34, P&lt;0.05) or in plasma (r = −0.42, P&lt;0.05). No association between sodium efflux rate constant and urinary sodium excretion occurred in normotensive subjects.
3. These findings provide further evidence that sodium is an important aetiological factor in hypertension. In ‘salt-sensitive’ individuals dietary sodium may interact with the regulation of cellular sodium transport via both humoral and cellular mechanisms to elevate blood pressure.
Effect of Sodium-Potassium-Dependent ATPase Inhibition on Noradrenaline-Activated Calcium Sensitivity of Mesenteric Resistance Vessels in Adult Spontaneously Hypertensive Rats
Authors: Mulvany M. J. , Nyborg N. , Nilsson H. 
Published: August 2015

1. We have investigated the noradrenaline-activated calcium sensitivity of 150 μm mesenteric resistance blood vessels from spontaneously hypertensive and control Wistar-Kyoto rats.
2. Under control conditions the spontaneously hypertensive rat blood vessels had a greater calcium sensitivity than the Wistar-Kyoto rat vessels.
3. In the presence of 1 mmol of ouabain/l, a treatment known to inhibit the sodium-potassium-dependent ATPase, the responses of the spontaneously hypertensive rat blood vessels were reduced more than those of the Wistar-Kyoto rat blood vessels, so that the responses of spontaneously hypertensive rat and Wistar-Kyoto rat blood vessels were then similar.
4. Similar results were obtained by removing external potassium, a procedure which should also inhibit the sodium-potassium-ATPase.
5. The results suggest that the greater noradrenaline-activated calcium sensitivity of spontaneously hypertensive rat blood vessels may be associated with an increased sodium-potassium-ATPase activity.
Pre- and Post-Junctional Adrenergic Mechanisms and Hypertension
Authors: Vanhoutte P. M. , Webb R. C. , Collis M. G. 
Published: August 2015

1. The ability of the blood vessel wall to synthesize noradrenaline is augmented at the early stages of genetic hypertension in animals. It usually is normal, or reduced in chronic hypertension.
2. The exocytotic release of noradrenaline is greater than normal, in the early stages of a number of experimental models of hypertension.
3. Postjunctional receptors for noradrenaline are not uniform throughout the vascular tree. Their sensitivity changes during the development of high blood pressure.
4. In chronic hypertension neuronal uptake and the extraneuronal disposition of released noradrenaline is depressed in the heart, but accelerated in the blood vessel wall.
5. The adrenergic neuro-effector interaction undergoes a diverging long-term adaptation in the heart and the blood vessels of hypertensive animals. In the former this tends to increase, but in the latter to reduce, the efficiency of sympathetic nervous control.
Dissociation between Central and Peripheral Noradrenergic Activity in Essential Hypertension
Authors: Lake C. R. , Polinsky R. J. , Gullner H.-G. , Ebert M. H. , Ziegler M. G. , Bartter F. C. , Kopin I. J. 
Published: August 2015

1. Eleven patients with essential hypertension and nine healthy normotensive volunteer subjects, all without a neurological disorder, had blood drawn and cerebrospinal fluid sampled for analysis of noradrenaline (NA).
2. Cerebrospinal fluid NA levels were elevated (P&lt;0.01) in the hypertensive patients but plasma levels of NA were similar between groups.
3. The results suggest there is noradrenergic hyperactivity in the central nervous system which is not reflected in abnormal peripheral sympathetic nervous system function in this group of patients.
A Hierarchical Organization of Blood Pressure during Natural Behaviour in Rat and the Effects of Central Catecholamine Neurons Thereon
Authors: Ledoux J. E. , Tucker L. W. , Del Bo A. , Harshfield G. , Green Lori , Talman W. T. , Reis D. J. 
Published: August 2015

1. Changes in arterial pressure associated with a repertoire of natural behaviour patterns in the rat were examined.
2. A hierarchy of such changes was found. Eating and drinking were associated with higher pressures than grooming and exploration, which in turn were associated with higher pressures than resting.
3. Desynchronized sleep was associated with higher pressures than slow-wave sleep.
4. Lesions of the catecholamine neurons of the A2 region of the medulla did not disrupt the normal hierarchy but resulted in an exaggerated pressor response.
Angiotensin Activates Sympathetic Reflexes in the Anaesthetized Cat
Authors: Clough D. P. , Hatton R. , Conway J. , Adigun S. A. 
Published: August 2015

1. Lower-body subatmospheric pressure has been used to stimulate sympathetic reflexes in anaesthetized cats and the effects of an angiotensin converting enzyme inhibitor and [Sar1, Ala8]angiotensin II have been investigated on this reflex.
2. At the prevailing level of renin activity (2.9-3.2 ng of angiotensin I h−1 ml−1) the converting enzyme inhibitor had no effect on blood pressure yet it potentiated the initial fall in blood pressure caused by the reduced pressure and it impaired its recovery. After 10 min, therefore, blood pressure was still reduced after converting enzyme inhibitor treatment whereas in control experiments full recovery occurred within 30 s.
3. When converting enzyme inhibitor was given 75 s after the start of a 10 min period of reduced pressure, at a time when plasma renin activity had not been increased, it caused a greater and more sustained fall in pressure than it caused when administered alone. The angiotensin II antagonist, [Sar1,Ala8]angiotensin II, produced similar effects.
4. These findings suggest that the renin-angiotensin system interacts with the sympathetic nervous system to maintain systemic arterial pressure.