bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on the Hypotensive Effect of High Potassium Intake in Patients with Essential Hypertension
Authors: Iimura Osamu , Kijima Toshiaki , Kikuchi Kenjiro , Miyama Akiyoshi , Ando Toshiaki , Nakao Takashi , Takigami Yoshiichi 
Published: August 2015

1. In order to confirm and investigate the hypotensive effect of a high potassium intake we compared mean arterial pressure (MAP), water and electrolyte balance, plasma and urinary noradrenaline (NA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in 20 inpatients with mild or moderate essential hypertension on a control diet (Na: 260, K: 75 mmol/day), and after high (K: 175 mmol/day) and low potassium diets (K: 25 mmol/day).
2. After potassium loading, urinary volume (UV) and urinary excretion of sodium (UNaV) and of potassium (UKV) were elevated, and MAP, body weight, plasma volume (PV), extracellular fluid volume (ECFV) and total exchangeable sodium (Nae) were reduced significantly.
3. After potassium loading, PRA, PAC, plasma and urinary NA increased and the pressor response to infused noradrenaline and angiotensin II decreased significantly.
4. The reduction of MAP after potassium loading correlated positively with PV and ECFV during the control period. In addition, significant correlations were found between ΔUV and ΔUNaV, —ΔPV and ΔU/NaV, —ΔPV and Δ plasma NA, and Δ plasma NA and Δ PRA.
5. Patients with low PRA had high PV, ECFV and Nae during the control period, and showed greater reductions of MAP, PV, ECFV and Nae after potassium loading.
6. After potassium restriction, UNaV, PRA and urinary NA decreased and PV increased, and MAP did not change significantly.
7. These results suggest that the hypotensive effect of high potassium intake may be caused by reduction of body fluid volume via augmentation of Na excretion.
Substrate Oxidation Shortly after Accidental Injury in Man
Authors: Little R. A. , Stoner H. B. , Frayn K. N. 
Published: August 2015

1. Oxidative metabolism has been studied by indirect calorimetry in 42 patients within the first 6 h after accidental injury.
2. the level of energy expenditure bore no relationship to the severity of the injury and varied more widely from patient to patient than in normal subjects.
3. After minor and moderate injuries the respiratory exchange ratio (mean 0.86) was not different from that in normal subjects on a mixed diet. After severe injuries the ratio (mean 0.78) was significantly lower (P &lt; 0.005), indicating that the main substrate for oxidation in these patients was fat, despite their hyperglycaemia.
Left Ventricular Hypertrophy Improves Cardiac Function in Spontaneously Hypertensive Rats
Authors: Lundin S. , Friberg P. , Hallbäck-Nordlander Margareta 
Published: August 2015

1. The influence of different arterial pressures on the relationship between diastolic filling pressure and stroke volume was studied during pharmacological cardiac nerve blockade in adult, anaesthetized spontaneously hypertensive rats in comparison with matched normotensive Wistar—Kyoto rats.
2. Peak stroke volumes, obtained by rapid blood volume expansion were similar in both types of rat, despite a more than 40% higher mean arterial pressure in the spontaneously hypertensive rats.
3. When peak stroke volumes were compared in the two groups at equal ‘normotensive’ or ‘hypertensive’ arterial pressures, they were always greater in the spontaneously hypertensive rats.
4. Calculation of diastolic wall/lumen ratios indicated that the increase of maximal stroke work in the spontaneously hypertensive rats closely matched the hypertrophic increase in wall/lumen ratio of the left ventricle.
5. These results indicate that left ventricular hypertrophy in established primary hypertension is a physiological adaptation to match left ventricular performance to the raised afterload.
Extent of Structurally Reduced Venous Distensibility in Rats
Authors: Nilsson Holger , Haraldsson Börje , Folkow Björn 
Published: August 2015

1. Venous pressure-volume relations were studied in maximally vasodilated whole-body preparations after cardiac arrest, as well as in fully vasodilated, perfused hindquarter preparations of spontaneously hypertensive rats (SHR) and normotensive controls. Central venous pressures were measured also in the anaesthetized animals before cardiac arrest.
2. Central venous pressure in intact, anaesthetized SHR was 1.9 ± 0.20 mmHg compared with 0.75 ± 0.25 in controls (P &lt; 0.001).
3. In both preparations SHR showed a nearly 20% reduction in venous compliance, whereas calculated ‘unstressed’ volumes (volumes at zero transmural pressure) were largely equal in SHR and controls.
4. SHR capacitance vessels thus appear to have a structurally reduced wall distensibility of about 10% with no change in overall size. It probably reflects a structural adaptation to a modest increase of average transmural pressure that also affects the low-pressure side.
Does Vasopressin Play a Role in the Pathogenesis of Hypertension?
Authors: Padfield P. L. , Brown J. J. , Lever A. F. , Morton J. J. , Robertson J. I. S. 
Published: August 2015

1. Plasma levels of vasopressin were found to be significantly higher in 29 patients with malignant hypertension than in 106 normotensive control subjects (13 ± 2 ng/l vs 5.8 ± 0.2 ng/l, P &lt; 0.001).
2. No correlation was apparent between blood pressure and circulating vasopressin.
3. An acute, incremental infusion of vasopressin (0.125, 0.25 and 0.5 ng min−1 kg−1) in nine patients with mild-moderate essential hypertension produced only minor changes in blood pressure despite achieving plasma levels spanning those seen in malignant hypertension.
4. Despite a small increase in pressor sensitivity to vasopressin in hypertensive subjects it is thus unlikely that an acute vasoconstrictor effect of this peptide is important in the pathogenesis of malignant hypertension.
The Reflex Control of Arginine-Vasopressin Release in Essential Hypertension
Authors: Ricciardelli B. , Volpe M. , Trimarco B. , Chiariello M. , Rengo F. , Condorelli Mario 
Published: August 2015

1. The reflex control of arginine-vasopressin release was studied in 12 essential established hypertensive patients and in 12 age-matched normal subjects by comparing the effects of head-up tilt and a variable-pressure neck-chamber.
2. After 45 min 85° head-up tilt, normal subjects showed an increase in plasma arginine-vasopressin and in plasma renin activity, while plasma volume decreased. In hypertensive patients, plasma arginine-vasopressin showed changes after tilt opposite to those of controls, while the changes in plasma renin activity and plasma volume were similar to those observed in the normal group. In both groups the changes in systolic and diastolic blood pressure were not statistically significant. A reduction in carotid sinus transmural pressure obtained by increasing neck-tissue pressure (+ 50 mmHg) by means of a neck-chamber, evoked different responses in mean blood pressure in the two groups, but failed to induce any significant change in plasma arginine-vasopressin concentration both in the normal and in the hypertensive subjects.
3. These results seem to suggest that carotid sinus baroreceptors, though active in blood pressure control, do not play a direct role in arginine-vasopressin release and, therefore, the opposite response of arginine-vasopressin observed after tilt in the two groups of subjects should be ascribed to more complex mechanisms.
Abnormalities and Drug-Induced Alterations of Vasopressin in Human Hypertension
Authors: Thibonnier M. , Aldigier J. C. , Soto M. E. , Sassano P. , Menard J. , Corvol P. 
Published: August 2015

1. Plasma vasopressin was estimated in 20 normotensive, 46 moderate hypertensive and 14 severe hypertensive patients under normal sodium diet.
2. In moderate hypertensive patients basal values for plasma vasopressin (PVP) after overnight dehydration and 24 h urinary vasopressin (UVP) were respectively 1.82 ± 0.23 pmol/l and 44 ± 4 pmol/day, which were not different from those found in normal subjects (PVP = 1.14 ± 0.11 pmol/l and UVP = 54 ± 4 pmol/day). In contrast, basal values were significantly increased in severely hypertensive patients (PVP = 4.69 ± 1.45 pmol/l, P &lt; 0.005; UVP = 107 ± 17 pmol/day, P &lt; 0.01).
3. In a group of 12 moderately hypertensive patients the blood pressure reduction induced by a single 20 mg dose of nifedipine was associated with an increase in PVP from 1.48 ± 0.57 to 2.48 ± 0.74 pmol/l (P &lt; 0.05) and in UVP from 42 ± 7 to 67 ± 17 pmol/day (P &lt; 0.05). On the other hand, a single dose of captopril (1 mg/kg body weight) administered to the same patients did not alter PVP (1.68 ± 0.43 pmol/l) and UVP (40 ± 6 pmol/day) despite a similar blood pressure decrease.
4. In a group of 10 severely hypertensive patients, the blood pressure reduction induced by the first dose of captopril (1 mg/kg) was correlated to the pretreatment level of PVP (r = 0.89, P &lt; 0.001) and of UVP (r = 0.70, P &lt; 0.01). Eight days of captopril treatment reduced PVP from 5.24 ± 1.38 to 1.18 ± 0.32 pmol/l (P &lt; 0.01) and UVP from 68 ± 17 to 25 ± 3 pmol/day (P &lt; 0.001).
5. Increased levels of vasopressin are a marker of severe forms of hypertension. The reduction of vasopressin during captopril treatment could be an additional mechanism underlying the anti-hypertensive effect of that drug. Moreover, from the comparison between nifedipine and captopril, it appears that antihypertensive drugs have different effects on vasopressin release.
Daily Profile of Baroreflex Sensitivity and the Variability of Blood Pressure in Essential Hypertensive Patients
Authors: Ogawa Jun , Arai Shiro , Takata Shigeo , Ikeda Takayuki , Takabatake Toshikazu , Hattori Nobu , Nomura Gakuji 
Published: August 2015

1. We have monitored intra-arterial pressure continuously throughout the day and analysed every beat by computer.
2. Baroreflex sensitivity (ms/mmHg) was measured four times a day (07.00, 12.00, 17.00 and 20.00 hours) in seven patients and three times a day (07.00, 12.00 and 17.00 hours) in 23 patients. The diurnal variation of baroreflex sensitivity in individual patients was 0–5.3 ms/mmHg and was not consistent. Mean baroreflex sensitivity was reduced in hypertensive patients compared with normotensive subjects.
3. A negative correlation was seen between baroreflex sensitivity and the variability of systolic blood pressure.
4. Baroreflex sensitivity was well correlated with the variability of heart rate.
Elevated Plasma Adrenaline Reflects Sympathetic Overactivity and Enhanced α-Adrenoceptor-Mediated Vasoconstriction in Essential Hypertension
Authors: Bolli P. , Amann F. W. , Hulthén L. , Kiowski W. , Bühler F. R. 
Published: August 2015

1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin.
2. Under basal conditions mean blood pressure (P &lt; 0.001), heart rate (P &lt; 0.01), forearm blood flow (P &lt; 0.001) as well as adrenaline concentration (P &lt; 0.01), but not noradrenaline, was higher in patients with essential hypertension.
3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P &lt; 0.001).
4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P &lt; 0.01). In the former the stress-induced increase in plasma adrenaline correlated with the increase in mean blood pressure (r = 0.514; P &lt; 0.05).
5. Prazosin increased forearm blood flow more in essential hypertension (P &lt; 0.001). This increase correlated with the resting plasma adrenaline in the hypertensive (r = 0.710; P &lt; 0.001), but not in normotensive, subjects.
6. When the cold pressor test was repeated during postsynaptic α1-adrenoceptor blockade forearm blood flow did not decrease; instead it increased further in both groups (P &lt; 0.05).
7. Thus in essential hypertension elevated plasma adrenaline concentration reflects sympathetic overactivity as also expressed by enhanced α-adrenoceptor-mediated vasoconstriction.
Blood Volume and the Carotid Baroreceptor Reflex in Conscious Rabbits
Authors: Ludbrook J. , Faris I. B. , Jamieson G. G. 
Published: August 2015

1. The effects of acute blood volume change in conscious rabbits on a.c. gain of the carotid baroreceptor reflex with respect to heart rate, blood pressure, cardiac output and systemic vascular resistance were studied.
2. With acute, isohaemic increase in blood volume by 20% and 40% the only consistent trend was a decrease in gain for systemic vascular resistance.
3. With acute reduction in blood volume there was a consistent tendency for gain for heart rate to fall. With 20% reduction in blood volume, gain for cardiac output fell but gain for systemic vascular resistance rose and its phase-lag became shorter, so that gain for blood pressure was unaltered. The enhanced gain for systemic vascular resistance was not sustained with 35% reduction in blood volume, so that gain for blood pressure fell.
4. Thus control of blood pressure by the carotid sinus reflex is remarkably unaffected by acute change in blood volume, and is impaired only when there is depression of gain for cardiac output without a concomitant rise in gain for systemic vascular resistance.
Contribution of Cardiovascular Reflexes to Differences in β-Adrenoceptor-Mediated Responses in Essential Hypertension
Authors: Jennings G. , Bobik A. , Esler M. , Korner P. 
Published: August 2015

1. The responses to stimulation of both cardiac and lymphocyte β-adrenoceptors were studied in 23 normal subjects and 23 with untreated essential hypertension. Lymphocyte cyclic adenosine monophosphate was measured in vitro after incubation with isoprenaline (0.01 μmol/l-10 mmol/l). There were no significant differences between the amount of cyclic adenosine monophosphate generated by lymphocytes in the two groups in the isoprenaline concentration range 0.01 μmol/l-1 mmol/l.
2. In the same subjects we compared cardiac β-adrenoceptor-mediated responses using the change in heart rate after bolus doses of isoprenaline (dose range 0.25–3 μg). In 12 subjects (six normotensive, six hypertensive) we studied the heart rate responses to isoprenaline before and after ‘total’ autonomic block (0.04 mg of atropine/kg and 300 μg of clonidine). The latter permitted assessment of intrinsic cardiac responsiveness after eliminating cardiovascular reflexes.
3. In subjects with reflexes intact the rise in heart rate was significantly greater in normal than in hypertensive subjects at all doses of isoprenaline. Isoprenaline evoked a similar dose-related fall in blood pressure in both groups, which contributed to the reflex drive. After autonomic block the differences in heart rate responses were no longer present.
4. The results indicate that the reduced tachycardia at a given dose of isoprenaline in hypertensive subjects is due to impairment in their baroreceptor—heart rate reflex since this was no longer present after atropine and clonidine.
5. The absence of any intrinsic difference in cardiac β-adrenoceptor responsiveness is in agreement with the results with lymphocytes.
Endogenous Agonist Regulation of α-Adrenoceptors in Man
Authors: Davies I. B. , Sudera D. , Sever P. S. 
Published: August 2015

1. Plasma noradrenaline concentrations and platelet α-receptor properties were measured in 14 normal subjects, five phaeochromocytoma patients and nine patients with multiple system atrophy and sympathetic nervous system degeneration (MSA).
2. Plasma noradrenaline concentrations in phaeochromocytoma were 10- to 20-times greater than those of normal subjects and one-fifth to one-half of normal in MSA patients.
3. Platelet α-receptor numbers were increased in MSA and decreased in phaeochromocytoma compared with normal subjects. There was no change in platelet α-receptor affinity in either group.
4. The inverse relationship between α-receptor numbers and plasma noradrenaline concentrations may reflect regulation of α-receptor number by endogenous adrenergic agonist concentrations in man.
Role of Dopamine in the Regulation of Blood Pressure and the Renin—Angiotensin—Aldosterone System in Conscious Rats
Authors: Kondo Kazuoki , Ebihara Akio , Suzuki Hiromichi , Saruta Takao 
Published: August 2015

1. In conscious rats, intracerebroventricular injection of dopamine resulted in a decrease in blood pressure, whereas injection of metoclopramide, the dopamine antagonist, produced an increase in blood pressure. The central depressor effect of dopamine was attenuated by a subpressor pretreatment with intraventricular metoclopramide, but not by phentolamine.
2. Intravenous administration of dopamine increased blood pressure. This increase in blood pressure was almost completely abolished by intravenous phentolamine. Metoclopramide, when injected intravenously, did not induce any change in blood pressure.
3. Plasma renin activity and plasma aldosterone concentration were decreased by intraventricular injection of dopamine, and increased by that of metoclopramide. In contrast, intravenous administration of metoclopramide increased plasma aldosterone concentration without changing plasma renin activity. Plasma concentrations of potassium, sodium and corticosterone were not affected by these treatments.
4. These results suggest that the dopaminergic system in the brain, but not in the systemic circulation, is involved in the regulation of blood pressure. It is also suggested that the central dopaminergic system participates in the regulation of aldosterone secretion by changes in the renin—angiotensin axis, whereas the peripheral dopaminergic modulation of aldosterone secretion appears to occur independently of the renin-angiotensin system.
Distribution and Properties of Angiotensin-Converting Enzyme in Cerebral Microvessels of the Rabbit and Rat
Authors: Brecher P. , Hingorani Vandana , Reininga Karen , Chobanian A. V. 
Published: August 2015

1. Angiotensin-converting enzyme (ACE) activity was threefold greater in isolated cerebral microvessels obtained from rabbit brain than rat brain.
2. ACE activity was distributed throughout the cerebral microvasculature, since differences were not found between preparations enriched in capillaries as compared with those enriched in arterioles and venules.
3. Aortic tissue from rat and rabbit had little ACE activity compared with the microvessels.
4. ACE activity was tightly associated with endothelial cells and was not released by heparin under conditions where lipoprotein lipase was effectively removed.
Activation of Renin in An Anaplastic Pulmonary Adenocarcinoma
Authors: Soubrier F. , Skinner S. L. , Miyazaki M. , Genest J. , Menard J. , Corvol P. 
Published: August 2015

1. Biochemical characteristics of a renin-like enzyme secreted by a pulmonary adenocarcinoma have been studied. A very high renin content was revealed by both enzymatic (10.4 Goldblatt units/g of tissue) and direct radioimmunoassay of immunoreactive renin (23 Goldblatt units/g of tissue).
2. The higher value by direct radioimmunoassay suggested the presence of an inactive form of the enzyme. Indeed 40–100% activation occurred with treatment by trypsin or pepsin or prolonged dialysis at pH 7.4 with or without prior acid dialysis. This neutral activation was completely abolished by a serine proteinase inhibitor.
3. A large fraction of the renin in this tumour is inactive. In comparison with other pro-hormones produced in tumours the findings support strongly the proposition that renin passes through a proenzyme step in synthesis.
Are Prostaglandins Involved in the Antihypertensive Effect of Dihydralazine?
Authors: Reimann Ingrid W. , Ratge D. , Wisser H. , Frölich J. C. 
Published: August 2015

1. Two female and two male patients with essential hypertension were given dihydralazine plus saline or dihydralazine plus diclofenac intravenously on two separate occasions. The dihydralazine dose (range: 16.2–32.4 mg/2 h) was chosen individually to reduce systolic blood pressure by 20 mmHg from the control value before the investigation; the intravenous diclofenac dose was 75 mg/20 ml of saline for all patients.
2. Dihydralazine decreased diastolic blood pressure more than systolic blood pressure and increased heart rate; diclofenac reduced both of these effects.
3. Dihydralazine increased urinary volume and sodium clearance; both these effects were antagonized by concomitant treatment with diclofenac.
4. Whereas dihydralazine did not influence creatinine clearance appreciably, concomitant administration of diclofenac reduced creatinine clearance.
5. Urinary prostaglandin E2 was reduced by diclofenac.
6. We suggest that dihydralazine-mediated vasodilatation is reduced by cyclo-oxygenase inhibition.
Effects of Bromocriptine on Blood Pressure and Plasma β-Endorphin in Spontaneously Hypertensive Rats
Authors: Hutchinson J. S. , Di Nicolantonio R. , Lim A. , Clements J. , Funder J. W. 
Published: August 2015

1. Immunoreactive β-endorphin (IR-βEP) was two- to three-fold higher in pituitary neuro-intermediate lobes (N-IL) of spontaneously hypertensive rats (SHR) than of normotensive Wistar—Kyoto (NT-WKY) controls.
2. Plasma levels of IR-βEP were lower in SHR than in NT-WKY rats.
3. Intravenous injections of morphine lowered blood pressure of both SHR and NT-WKY rats to the same level; naloxone restored blood pressure of both groups to pre-morphine values.
4. Infusion of bromocriptine in SHR for 1 week lowered blood pressure and N-IL IR-βEP concentration.
5. These results confirm and extend postulated dopaminergic defect in this model of hypertension.
Experimental Essential Hypertension in the Rat?
Authors: Nowaczynski M. , Nowaczynski W. , Mavoungou D. , Wilkins G. , Fung K. , Boyko R. 
Published: August 2015

1. A human urinary thermostable glycoprotein (ABG-TsU) believed to be a homologue of the plasma aldosterone-binding globulin (ABG) was isolated and purified by differential ultra-filtration, ion-exchange chromatography and gel filtration to electrophoretic homogeneity; it showed a charge heterogeneity in electrofocussing.
2. ABG-TsU was administered intraperitoneally to male rats in small daily doses (7 μg/day per rat). Sustained hypertension developed in 5–8 days.
3. The treated rats showed no changes in plasma electrolytes, aldosterone or plasma renin activity; however, a significant increase in heart weight was observed.
4. This hypertension appears to be adrenal dependent since it is prevented by bilateral adrenalectomy or administration of an aldosterone antagonist, but not by adrenalectomy when aldosterone is given concomitantly with ABG-TsU.
HLA Antigens in Spanish Patients with Essential Hypertension
Authors: Fernandez-Cruz A. , Otero M. Luque , Perez L. Llorente , Pinilla C. Fernandez , Claros N. Martell 
Published: August 2015

1. Human leucocyte AB antigens were determined by means of a lymphocyte toxicity test in 84 patients with essential hypertension and in 1000 blood donors.
2. The prevalence of HLA B8 was 16.4% in hypertensive patients and 8.9% in controls (P = 0.07).
3. The prevalence of HLA B12 was 34.5% in hypertensive patients and 26.9% in the control group (N.S.). In WHO stage III hypertension HLA B12 was found in six out of 10 patients.
4. The prevalence of HLA B15 was 1.2% in hypertensive patients and 6.4% in controls (P &lt; 0.05).
5. In view of a previous report of HLA antigens in a Spanish diabetic population, this study does not support the suggestion of a genetic and possibly HLA-linked connection between essential hypertension and diabetes mellitus among the Spanish population.
6. A positive family history of hypertension tended to be more common in those patients with essential hypertension associated with HLA B8.